Summary Biological psychology by Kalat (11th edition)

Chapter 1 - Introduction

What is the relationship between mind and body?

Biological Psychology is the study of the physiological, evolutionary, and developmental mechanisms of behavior and experience.

There are four categories of biological explanations of behavior:

1. The Physiological explanation focuses on the brain and other anatomical structures.

2. The Ontogenetic explanation focuses on the development of structures/behavior.

3. The Evolutionary explanation focuses on the evolutionary history of structures/behavior.

4. The Functional explanation focuses on the functions of structures/behavior, why they developed.

The mind-body problem asks the question: What is the relationship between between mental activity and brain experience? There are two different approaches to this question:

1. Dualism is the view that the mind and body function separately.

2. Monism is the view that the mind and body are the same substance. We can identify various forms of monism: materialism (everything is physical) mentalism (the mind is a precondition for the physical world) and identity position (the mind and body are the same but described by different terms).

Do other people have consciousness?

Solipsism is the belief that “I am the only one who exists”.

Easy and hard problems of consciousness

The genetic basis of behavior

Genes are units of heredity, which come in pairs. Chromosomes are strands of genes and they also occur in pairs (with the exception of a male mammal who has unpaired X and Y chromosomes).

DNA (deoxyribonucleic acid) is a molecule which contains genetic instructions. Its function is to work as a model for the RNA synthesis (RNA a.k.a ribonucleic acid).

• DNA is a double-stranded molecule, RNA is one-stranded.

• RNA molecule works as a model for protein synthesis.

• Proteins either form the structure of the body or work as enzymes which are proteins that catalyze chemical reactions in the body.

• An individual can be either homozygous or heterozygous for a certain gene, depending whether s/he has an identical (homozygous) pair of genes or unmatched pair of genes on the two chromosomes.

Genes are either dominant, recessive, or intermediate:

1. Dominant genes express what they code in every case (so, both in homozygous and heterozygous conditions).

2. Recessive genes express what they code if the two chromosomes are identical (so, only in homozygous condition).

3. Intermediate genes expression of the trait is a result of the interaction by the genes of both parents.

Chromosomes are either:

1. Sex chromosomes (where the sex-linked genes are).

2. Autosomal chromosomes (all other chromosomes).

Sex chromosomes are named X and Y. Women have chromosomes XX and men have chromosomes XY.

1. Genes that are carried by either sex chromosome are said to be sex linked.

2. Sex-limited genes are genes which are present in both sexes but turned on in only one sex.

Heredity versus environment

Classic dilemma, but the conclusion is that every behavior is caused by both heredity and environment!

• The implications of heredity and environment can be studied by comparing monozygotic (having shared one zygote and therefore identical) and dizygotic twins or adopted children.

• Researchers have also found connections between certain genes and disorders.

• A distinction between the environmental and hereditary factors is difficult for several reasons. The prenatal (before birth) environment has its effects on the child. Sometimes a methyl group can attach to a gene and inactivate it.

• There is interaction between behavior and the environment: a multiplier effect which states that genetics produce a small increase in some behavior, when the environment starts to magnify that tendency.

• Even inherited traits can be modified by the environment.

• Genes do not cause certain behaviors, but they can increase their probability.

• Evolution is the change over time in one or more inherited traits found in populations.

• Artificial selection describes intentional breeding for certain traits, or combination of traits. It is the opposite for natural selection.

• Genes do not change in accordance to usage of certain body parts.

• Genes are ‘selfish’ in that they try to multiply and evolution works for them.

• Evolutionary psychology examines psychological traits from a modern evolutionary perspective. It seeks to identify which human psychological traits are evolved adaptations.

• The concept of altruistic behavior causes a dilemma for evolutionary psychology.

• Reciprocal altruism (people help those who are able to help them back) is one attempt to solve the problem.

• Another explanation is kin selection (we favor the reproductive success of our relatives, even at a cost to our own survival and/or reproduction).

Animals in research

There are several reasons why animals are used as test subjects instead of humans:

1. It is unethical to conduct certain studies using humans.

2. Through the study of animals we gain knowledge about human evolution.

3. Animals are interesting in themselves.

4. Animals are similar to humans in many ways, and often it is easier to use animals.

Animal research will be a part of neuroscientific research in the future. Most of the researchers claim that a little harm should be tolerated for the sake of greater good.

Without animal research many serious diseases might remain uncured. However, there are also alternatives to animal testing.

People against animal research hold different kind of positions:

1. Minimalists think that animal research should be firmly restricted. Justification depends on the expected value of the research, the level of harm to the animal, and the type of animal.

2. Abolitionists think that all animals are equal to humans, so animal testing is never justifiable.

The legal standard is “the three Rs”

1. Reduction of the number of animals.

2. Replacement, in other words the use of substitutes (e.g. computer models) for animals whenever possible.

3. Refinement, in other words reducing pain and discomfort as much as possible.

Universities and other institutions have committees to control animal testing.

Chapter 2 - Neural cells

The cells of the nervous system

The nervous system consists of two kind of specialized cells:

1. Neurons: process and transmit information by electrical and chemical signaling.

2. Glia: maintain homeostasis, form myelin, provide support and protection for neurons

An adult has approximately 100 billion neurons. Neuroscience is a relatively new branch of science. Charles Sherrington and Santiago Ramón y Cajal are considered to be the main founders of neuroscience.

The structure of a neuron is very much similar to the other animal cells. Most of the animal cells share the following structures:

1. The nucleus serves as the control center of a cell and contains the cell's chromosomal DNA.
2. Mitochondrion perform metabolic activities and is akin to a cellular 'power plant'.
3. Ribosome creates proteins.

Usually a neuron has four parts:

1. Axon, a long branch of a neuron that conducts electrical impulses away from the soma.

2. Soma (also called the cell body), contains the nucleus and other basic structures.

3. Dendrites, branched projections that conduct electrical impulses received from other neurons to the soma.

4. Presynaptic terminals, specialized junctions through which neurons signal to each other.

The myelin sheath is an insulating layer around the axon. It has intervals called the nodes of Ranvier. The myelin sheath accelerates the action potential. An afferent axon is an axon that imports information into a structure. An efferent axon is an axon that exports information from a structure. An Interneuron is a neuron that connects afferent neurons and efferent neurons in neural pathways.

Glial cells, sometimes called neuroglia, are non-neuronal cells with several functions:

1. Astrocytes support endothelial cells that form the blood-brain barrier, syncronise the activity of the axons, control the blood flow and remove waste material.

2. Microglia work as an immune defence in the nervous system by removing waste material and viruses.

3. Oligodendrocytes insulate the axons by building the myeling sheath.

4. Schwann cells work as oligodendrocytes.

5. Radial glia control and guide the migration of neurons.

The vertebrate brain does not replace damaged neural cells, as damaged cells in the other parts of the body are being replaced. This is why we need a blood-brain barrier.

The blood-brain barrier blocks out most viruses, bacteria and harmful chemicals. However, it also blocks out most nutrients and for consequently many medications.

Some chemical can cross the blood-brain barrier:

1. Small uncharged molecules (e.g. oxygen, carbon dioxide).

2. Water (via special protein channels).

3. Molecules that dissolve in the fats of the membrane.

Some other essential chemicals are actively transported into the brain. These chemicals include glucose (energy source), amino acids, choline, some vitamins, purines, iron and some hormones.

A virus that manages to enter the nervous systems probably stays there (e.g. rabies, herpes).

The Action Potential

Nerve impulse is an action potential. It is an event in which the electrical membrane potential of a cell rapidly rises and falls.

Electrical gradient refers to the difference in electrical charge between the inside and outside of the cell. The inside of a cell in the phase of the resting potential is negatively charged (approximately 70mV). Resting potential is the difference in electrical charge in a resting neuron. Can be measured using microelectrode. Concentration gradient is the difference in distribution of ions across the membrane. Molecules tend to move from areas of greater concentration to areas of lesser concentration. Polarization is the difference in electrical charge between e.g. inside and outside the cell. The charge inside the neuron is slightly negative because of the charged proteins.

Voltage-gated channel is a membrane protein controlling sodium entry. At the time of depolarization those channels open. Still even during the peak of the action potential the difference between concentrations remain.

After the action potential voltage-gated potassium channels open, sodium carries a positive charge out of the axon and the membrane returns to the phase of resting potential.

Local anesthetic drugs change the sodium channels of the membrane and prevent the flow of sodium ions (thus blocking action potential).

The All-or-none law states that the strength by which a nerve fiber responds to a stimulus is not dependent on the strength of the stimulus. If the stimulus is any strength above threshold, the nerve or muscle fiber will give a complete response or otherwise no response at all. However, the greater the frequency of action potentials, the greater the intensity of the stimulus. The refractory period is the time after action potential when the cell resists further action potentials.

This can be divided into the absolute refractory period (approximately 1 ms, when the action potential is impossible in any case) and the relative refractory period (extra 2-4 ms, when the new action potential requires greater stimulus).

Chapter 3 – Communication between neurons

The synapse

A synapse is a junction that permits a neuron to pass an electrical or chemical signal to another cell.

A reflex is an involuntary and nearly instantaneous muscular movement in response to a stimulus.

A reflex arc is a neural pathway from sensory neuron to muscle response.

The velocity of the conduction through a reflex arc is less than through an axon: this happens because of synapses, when the neurons communicate with each other.

Temporal summation is when repeated stimuli in a short time have a cumulative effect.

Spatial summation is summation over space: one weak stimulus can not reach the threshold, but the combination of two similar stimuli located in different places can do it. This summation is essential for brain functioning.

Presynaptic neuron deliver synaptic transmission.

Postsynaptic neuron are in turn the receiving neuron.

Excitatory postsynaptic potential (EPSP) is the temporary depolarization of a membrane (sodium gates are open).

Inhibitory postsynaptic potential (IPSP) is the temporary hyperpolarization of a membrane (potassium or chloride gates are open).

Inhibition is not a lack of excitation, but it actively works against it.

Inhibitory neurons can work as a regulator to the timing of activity.

Chemistry of a synapse

The communication between neurons is based on chemical transmission.

Chemical events at a synapse occur in the following steps:

1. Action potential travels along the membrane of the presynaptic cell, until it reaches the synapse.

2. The electrical depolarization of the membrane at the synapse causes channels (for calcium ions) to open.

3. Calcium ions flow through the presynaptic membrane, rapidly increasing the calcium concentration in the interior.

4. The high calcium concentration activates a set of calcium-sensitive proteins attached to vesicles that contain a neurotransmitter chemical.

5. The vesicles open and dump their neurotransmitter contents into the synaptic cleft, the narrow space between the membranes of the pre- and post-synaptic cells.

6. The neurotransmitter diffuses within the cleft. Some of it escapes, but some of it binds to chemical receptor molecules located on the membrane of the postsynaptic cell.

7. The binding of neurotransmitter causes the receptor molecule to be activated in some way. This is the key step by which the synaptic process affects the behavior of the postsynaptic cell.

8. Due to thermal shaking, neurotransmitter molecules eventually break loose from the receptors and drift away.

9. The neurotransmitter is either reabsorbed by the presynaptic cell, then repackaged for future release, or else it is broken down metabolically.

Neurotransmitter transmits signals from a neuron to a target cell across a synapse. More than hundred transmitters have been identified, some major categories are:

1. Acetylcholines.

2. Monoamines.

3. Purines.

4. Gases.

5. Amino acids.

6. Neuropeptides.

Synthesis of trasmitters is based on substances in a diet.

• Neurotransmitter molecules are packed in vesicles, but the presynaptic terminal also has neurotransmitters outside the vesicles.

• MAO (monoamine oxidase) is an enzyme in serotonin, dopamine and norepinephrine, which breaks down these transmitters into inactive chemicals. The function of several antidepressant drugs is to inhibit MAO.

• Calcium in presynaptic terminal causes exocytosis (release of transmitter). After that the neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane, where it attaches to a receptor.

• Neurons release different kinds of neurotransmitters from different branches of their axons. However, neurons can receive and respond to many neurotransmitters at different synapses.

• The effect of a neurotransmitter also depends on the receptor. Some neurotransmitters cause an ionotropic effect, some cause a metabotropic effect.

• An ionotropic effect is a special kind of rapid effect of a hormone on its target.

• Metabotropic effect is slower and lenghtier than ionotropic effect.

• Ionotropic and metabotropic effects are linked to different kinds of behavior: ionotropic effets are related to vision and hearing, as metabotropic effects are more related to feelings, e.g. hunger, anger and fear.

• Also their transmitters are different; ionotropic effects use glutamate or GABA (gamma-amino butyric acid, metabotrophic effects use several transmitters).

• A synapse can have two kinds of channels: transmitter-gated or ligand-gated.

• Neuropeptides (also neuromodulators) are neurotransmitters that differ from other neurotransmitters in some ways: they are not released by axon terminal but by cell bodies and dendrites. It also requires consecutive stimulation.

• A hormone is a secreted chemical messenger that transports a signal from one cell to another.

• The difference between hormones and neurotransmitters is that neurotransmitters convey the message to a certain receiver whereas hormones send it to all over the body.

• Endocrine glands secrete their hormones directly into the blood rather than through a duct.

Some relevant endocrine glands and their hormones:

• Thymus: thymosin.

• Thyroid glands: thyroxine.

• Parathyroid glands: parathyroid hormone.

• Liver: somatomedins.

• Adrenal gland: aldosterone, cortisol.

• Kidney: rennin.

• Pancreas: insulin.

• Ovary (female) / testis (male): estrogens, androgens.

• Placenta (female during pregnancy).

• Hypothalamus: various releasing hormones (increase the release of other hormones).

• Pineal gland: pineal gland.

• Pituitary gland (divided into anterior pituitary and posterior pituitary): somatotropin (growth hormone), prolactin, and oxytocin.

After use, a neurotransmitter needs to be inactivated so that it won’t keep on exciting or blocking the receptor. This can happen in several ways:

1. Decomposition caused by an enzyme, e.g. acetylcholine is broken down by acetylcholinesterase.

2. Separation from the receptor, e.g. serotonin and catecholamines.

3. Detached transmitter can be used again via reuptake. Reuptake happens through membrane proteins called transporters.

4. Diffusion away, e.g. neuropeptides.

A negative feedback in the body is where a change in the level of one chemical leads directly to a reduction in its formation, reduction in its absorption, or increase in its excretion. Negative feedbacks are important in maintaining homeostasis in the body.

Autoreceptors take care of negative feedbacks.

Substance abuse

Many abused drugs are natural and can be derived from plants.

Drugs increase or inhibit transmission at synapses: antagonistic drugs block a neurotransmitter, agonistic drugs mimic or increase the effects of a neurotransmitter.

Drugs have different properties:

1. Affinity relates to what degree it binds to a receptor.

2. Efficacy is the tendency to activate the receptor.

Psychologists Olds & Milner (1954) accidentally found a brain area connected to nucleus accumbens (plays an important role in pleasure, addictions, reward etc. --> release of dopamine).

Most of the abused drugs increase the release of dopamine and norepinephrine.

When it comes to addictions, the question is how much you want something, not how much you like something.

Stimulant drugs increase excitement, happiness, alertness, activity. They also impair attention and learning.

Some examples of stimulant drugs are:

1. Amphetamine, which increases the release of dopamine.

2. Cocaine, which blocks the reuptake of dopamine.

3. Methylphenidate (Ritalin), used for attention-deficit disorder (ADD), blocks the reuptake of dopamine.

4. Methylenedioxymethamphetamine (MDMA, ecstasy), increases the release of dopamine and serotonin.

Opiates (e.g. morphine, heroin, and methadone) are derived from poppy seeds. They work as painkillers and relaxants. In 1973 researchers found opiate specific receptors and they realized that the human body must have its own chemical attaching these receptor. Indeed, soon they found endorphins (neuropeptides that indirectly activate dopamine release, by inhibiting the release of GABA, a transmitter that inhibits the firing of neurons).

• Marijuana contains cannabinoids, which are used as painkillers, to treat nausea or glaucoma and to increase appetite. Psychological effects: feeling that time has slowed down, impairment of memory, intensification of sensory experience.

• Cannabinoid receptors are very abundant receptors in the brain. Two natural brain chemicals attach to cannabinoid receptors: anandamine and 2-AG, which are released as retrograde transmitters (they travel back to incoming axons and inhibit further transmitter release).

• Hallusinogenic drugs (e.g. lysergic acid diethylamide aka LSD) are similar to serotonin.

• Small amounts of alcohol can help people to relax and prevent heart diseases, greater amounts damage liver and other organs and can lead to alcohol dependence in a long run.

• Alcohol affects GABA and glutamate receptors decreasing brain activity. It also increases stimulation at dopamine and opiate receptors.

Two types of alcoholism have been distinguished:

1. Type 1 alcoholism, gradual development, normally after age of 25.

2. Type 2 alcoholism, rapid onset, normally before age of 25. More common in men and linked to alcohol problems in close relationships.Certain genes are related to alcoholism, also prenatal environment affects the risk of alcoholism.

• Some effects of alcohol are greater for sons of alcoholics, e.g. it decreases stress more. Sons of alcoholics also show less intoxication after drinking than average. Furthermore, they have some abnormalities in their brain, e.g. smaller amygdala.

• After prolonged use of a substance, tolerance develops. Still even when the gained pleasure declines, the motivation to avoid displeasure fuels an addiction.

• Withdrawal symptoms of alcohol include shaking, sweating, nausea, hallucinations, convulsions and cardiovascular problems.

• Withdrawal symptoms of nicotine include irritability, insomnia, concentration difficulties and headaches.

• Craving for a substance continues after the end of withdrawal symptoms, maybe because addicts learn that a substance can be strongly enticing during sever stress or because addicts learn to associate several cues with a drug.

• In addicts, the nucleus accumbens responds less than usual to other incitements.

• Joining a group such as Alcoholics Anonymous or Narcotics Anonymous can help to overcome the addiction. Psychotherapy can be helpful too.

• In the body alcohol is metabolized to acetaldehyde, which is then converted to acetic acid by acetaldehyde dehydrogenase. Some people have a weaker genetic disposition for acetaldehyde dehydrogenase and therefore they easily get sick after drinking too much alcohol.

Several drugs are used to treat alcoholism:

1. Disulfiram (trade name Antabuse), antagonizes the effects of acetaldehyde dehydrogenase, and so the patient will get sick if s/he drinks.

2. Naloxone (trade name Revia), blocks opiate receptors (weakens the pleasure).

3. Acomprosate (trade name Campral), helps to cope with the withdrawal period.

Medications work only for people who really want to stop using alcohol.

Some drugs have been developed in order to work as a substitute for opiates. Methadone is similar to heroin and opiates but less harmful, the effect and the withdrawal symptoms are gradual. Also buprenorphine and levomethadyl acetate are used, and they can improve drug addict’s lives big time. However, they do not end the addiction.

Chapter 4 – Brain Anatomy

Each part of the nervous system has specialized functions. The cerebral cortex is the largest structure and elaborately processes sensory information and provides fine control of movement. How do the areas work together? Neuroanatomy is the anatomy of the nervous system.

Structure of the Vertebrate Nervous System

Each brain area and each neuron has a specialized role, but they also depend on the cooperation with other areas. The brain and the spinal cord make up the central nervous system. The peripheral nervous system consists of nerves which run through the whole body. The somatic nervous system is the part of the PNS, that transmits messages from the sense organs to the brain and also from the brain to the muscles. The autonomic nervous system is the part of the PNS which controls the heart, intestines, and other organs. Its cells are in the brain, the spinal cord and along the spinal cord.

We can look at an object (like the brain) from the following perspectives: dorsal (looking frontally towards the back), ventral (looking from behind towards the chest). In brain anatomy, a structure is anterior of another, when it is closer to the forehead (closer to the front end) and posterior, when it lies further away from it (toward the rear end). A part is superior to another, when it is above and inferior when it is below another structure. There are three ways of taking a plane through the brain: horizontal (cut horizontally to see upward or downward), sagittal (cut vertically from front to back to see structures from the side), or coronal (cut horizontally from ear to ear).

Two structures are ipsiateral, when they are in the same body hemisphere and contralateral when one is left, one is right. A point is lateral of another when it is further away from the midline, more toward the side of the object investigated and medial when it is closer towards the midline. A proximal point is close to something else whereas a distal point is further away.

The bulges in the cerebral cortex are called gyri. The grooves between them are called sulci (a deep sulcus is a fissure). A ganglion is a cluster of neuron cell bodies, usually outside the CNS. A nucleus is a cluster of neuron cell bodies within the CNS. A nerve is a set of axons. A lamina is a layer of nuclei which is separated from other nuclei by axons and dendrites. Columns are vertically arranged structures which share common characteristics (e.g. function). A group of axons which connects two cells and continuously projects from the sending to the receiving one is called a track.

Grey matter consists of cell bodies and dendrites, white matter of myelinated axons. The spinal cord is the part of the CNS within the spinal column. It communicates with all sense organs and muscles (except those of the head). Each segment has a sensory (dorsal location) and a motor (ventral location) nerve. The Bell-Magendi law first stated that the dorsal nerves carry sensory information while the ventral nerves carry motor information. The cell bodies of the sensory neurons are arranged in clusters of neurons outside the spinal cord, called the dorsal root ganglia. Cell bodies of the motor neurons are inside the spinal cord. The grey matter whithin is H-shaped. If the spinal cord is cut, there is no sensual perception and motor control over the area below the cut segment.

The autonomic nervous system consists of the sympathetic (responsible for fight or flight reactions, located next to the center of the spinal cord, work in synchrony, uses neurotransmitter norepinephrine) and parasympathetic (responsible for relaxation, located along the spinal cord close to each organ, work more independently, uses acetylcholine) nervous system. As they rely on different chemicals, different drugs affect them.

Forebrain, the midbrain and the hindbrain.

The hindbrain, the posterior part of the brain, consists of the medulla, pons and the cerebellum. The structures there (except the cerebellum) make up the brainstem. The medulla controls vital reflexes (e.g. breathing, heart rate) through the cranial (head) nerves. Damaging it is very dangerous. The pons is a functional bridge of the brain, where axons from each half of the brain cross to the opposite side. The raphe system sends axons to the forebrain, modifying the brain’s readiness to respond to stimuli. The cerebellum is the large hindbrain structure involved in movement, balance, attention and timing. The limbic system around the brain stem is important for motivation and emotions.

The midbrain lies in the middle of the brain. Its roof is the tectum. The sides of the tectum are the superior and inferior colliculus important for sensory processing. The substantia nigra gives rise to a dopamine-containing pathway that facilitates readiness for movement.

The forebrain consists of two hemispheres, either of which controls the contralateral side of the body. The outer portion is the cerebral cortex. The thalamus, right under it, is its major source of input. The thalamus is a pair of structures in the center of the forebrain. Most sensory information first goes here and is then sent to the cerebral cortex. Sending back and forth focusses attention on particular stimuli. The hypothalamus conveys messages to the pituitary gland, altering its release of hormones. The basal ganglia, lateral to the thalamus, is involved in movement, learning and remembering. The nucleus basalis, part of the basal forebrain, is involved in arousal, wakefulness and attention. The hippocampus, between the thalamus and the cerebral cortex, stores memory, especially those of individual events.

The four ventricles are filled with cerebrospinal fluid, which is also found in the meninges, the membrane surrounding the brain. Pressure on it leads to a painful perception. The fluid cushions the brain against mechanical shock when the head moves.

The Cerebral Cortex

The cerebral cortex is the outer layer one sees when opening a skull. Its two hemispheres communicate through the corpus callosum and the anterior commissure. The cerebral cortex is organized similarly in mammals and occupies 13% of the brain in mammals. It contains six distinct laminae (separate layers of cell bodies parallel to the surface) differently thick in different areas. Each lamina has different functions and pathways from where they go where. Cells of the cortex are also organized in columns of cells orthogonal to the laminae. Each column reacts to a distinct body part.

The occipital lobe (fpOt) at the posterior end of the cortex is responsible for vision. The posterior pole is the primary visual cortex/striate cortex. Cortical blindness/blindsight occurs after damage to this area, not the eyes.

The parietal lobe (fPot) lies between the occipital lobe and the central sulcus (the last area of which is the postcentral gyrus including the primary somatosensory cortex responsive to touch). The postcentral gyrus consists of four bands, each of them (showing one type of stimulation) representing the body. The parietal lobe monitors all information about eye, head, and body positions and numerical information.

The temporal lobe (fpoT) processes auditory information, language most in the left lobe. It also contributes to vision, such as perception of movement and face recognition. A tumor here can make up visual and auditory hallucinations. It is also involved in emotional and motivational behaviors.

The frontal lobe (Fpot) contains the primary motor cortex and prefrontal cortex. The precentral gyrus is responsible for fine movements. The larger a species cerebral cortex, the higher the percentage of the prefrontal cortex it occupies. Neurons here have 16 times more dendrites, resulting in huge amounts of information being processed. Working memory occurs here as well as making decisions and planning movements. Damage here impairs performance on the delayed-response task.

Prefrontal lobotomy was a 20^th century operation disconnecting the prefrontal cortex from the rest of the brain to “tame” people with psychological disorders. Most were performed by the founder, Freeman. Patients often became dull and apathetic, lost memory, became distractable and showed weird emotional expression.

The question of how various brain areas produce a perception of a single object is called the binding problem. Association areas rather perform advanced processing on a particular sensory system, such as vision or hearing, but few cells combine one sense with another. We can’t yet fully explain binding, but for it to occur we must perceive two stimulations as happening at the same time and place.

Research Methods

Brain damage can show which function a damaged part had. On lab rats ablations (removal or a brain area) and lesions (damages by a stereotaxic instrument-electroshock) are performed to find out about functions of brain areas. After death of the animal the brain is cut in slices and analyzed as to find out which area exactly had been damaged to verify the resulting outcomes. Sham lesions are performed to compare if the effect might not rather develop because of the operation than the electric lesion. The gene-knockout approach uses biochemical methods to direct a mutation to a particular gene important for certain types of cells, transmitters, or receptors.

Stimulation of certain brain areas shows connections between behavior and brain activity. Transcranial magnet stimulation, the application of a strong magnetic field to a portion of the scalp temporarily inactivates neurons below the magnet.

Optogenetics shine laser light within the brain to activate neurons. Mild stimulations enhance brain activity, but artificial stimulation produces artificial responses. It is easier to discover which brain area is responsible for e.g. vision than to discover how it produces a meaningful pattern.

Recording brain activity during tasks shows which brain areas get activated. An EEG (electroencephalographs) records electrical activity of the brain through electrodes attached to the scalp. The electrodes measure the average activity at any moment for the population of cells under it. They can measure spontaneous or evoked potentials (responses to a stimulus). An MEG (magnetoencephalograph) works similar, but measures a magnetic field rather than electrical activity. Both procedures locate activity within a centimeter. A PET (positron-emission tomography) provides a high-resolution image of activity in a living brain by recording the emission of radioactivity from injected chemicals. Areas showing most radioactivity are the most active one (with the biggest blood flow). This is mainly replaced by fMRI (functional magnetic resonance imaging) that makes scans that record the energy released by hemoglobin molecules after removal of a magnetic field. Hemoglobin with oxygen reacts to a magnetic field differently than without oxygen, and as working areas of the brain consume oxygen, brain activity can be shown. This procedure is accurate and quick. To see which areas are active during a task, 2 images are made: without a stimulus and then with the stimulus – the differences show the area responding to the stimulus. But areas in the brain have more than one function and we have to be cautious with making inferences. To some extend it is possible to “read someone’s mind” with fMRI.

Correlating brain anatomy with behavior can be interesting when observing unusual brains behavior and then looking for unusual brain features. In the 1800s Franz Gall invented phrenology, which is relating skull anatomy to behavioral features. But actually there is little relationship. CT scans (computerized axial tomography) take x-rays of the brain to detect tumors or structural abnormalities. MRI (magnetic resonance imaging) applies a strong magnetic field for a short time, activating neurons and afterwards evaluates activity. This can show tiny details in brain anatomy.

In people with special skills, particular brain areas are enlarged, but not the skull above it.

Neither brain mass nor brain-to-body ratio puts human in the first place asking whether brain size is correlated with intelligence. Each species is intelligent in its own way.

When comparing brain size with intelligence, there can be an effect found, when the genders are observed separately. A given task may activate different areas in different people simply, because they approach the task in different ways. That is, a given task (even an IQ test) may be in fact a different task for different people.

Men’s brains are generally bigger and heavier (because of more white matter) than women’s, but they have the same capacities in all areas. Differences in brains between sexes are based on differences in interest and cultural influences.

Chapter 5 - Development of the brain

Development of the Brain

Weight of the brain at birth is approximately 350g, at adulthood it ranges from 1200g to 1400g. Anatomy of the brain is plastic: it is changing constantly. The central nervous system start to form when the embryo is 2 weeks old. The brain and spinal cord start growing as folding lips surrounding a fluid-filled canal. The brain emerges during embryonic development from the neural tube, an early embryonic structure. The fluid-filled cavity within the neural tube becomes the central canal of the spinal cord and the four ventricles of the brain. It contains the cerebrospinal fluid (CSF).

Five processes in the development of neurons:

1. Proliferation, production of new cells. Some cells (stem cells) keep their location and continue dividing, others differentiate as primitive neurons or glia.

2. Migration, moving to other location. Migration is guided by immunoglobulins and chemokines. The brain has several kinds of these chemicals, which means that many things in development can go wrong but also that the absence of one chemical can be compensated by another.

3. Differentiation, primitive neurons form their axons and dendrites.

4. Myelination, the process in which glia produce the insulating fatty sheaths (to accelerate transmission).

5. Synaptogenesis, formation of synapses. This process continues the whole lifetime.

New neurons do not form in the adult cerebral cortex. Still, the brain can develop some new neurons, e.g. olfactory receptor neurons.

Stem cells in the brain remain immature the whole life, and they can also differentiate into new neurons in the adult hippocampus.

As people get older their neurons become less changeable, and therefore learning gets more difficult.

How do axons find their way to their target locations? They achieve this by following a chemical trail. Once they find their target location they arrange themselves over the area, after this the postsynaptic fine-tunes the connections by accepting certain combinations of axons.

Neural Darwinism: synapses form randomly and the process of selection keeps some and rejects others. However, in evolution mutations are random events but when it comes to neurons neurotrophins guide axonal branches in the right direction.

The sympathetic nervous system forms much more neurons than it needs and muscles determine how many of them survive.

Consequently, when a neuron forms a synapse onto a muscle, the muscle delivers a protein nerve growth factor (NGF).

If the neuron does not receive NGF, it will end up in process called apoptosis (programmed cell death).

This system explains how the number of incoming axons and receiving cells are matched.

Neurotrophins are a family of proteins that induce survival development, and the function of neurons. Also NGF and brain-derived neurotrophic factor (BDNF) are neurotrophins.

• While releasing neurotransmitters, neurons also release neurotrophins.

• Loss of neurons is a normal part of development, and actually it can be a sign of maturation.

• The brain is extremely sensitive to many substances in the early phases of development. Several factors can lead to impairment: toxic chemicals (e.g. alcohol), infections, malnutrition, stress etc.

• Fetal alcohol syndrome (FAS) is a pattern of mental and physical defects that can develop in a fetus when a woman drinks alcohol during pregnancy. Symptons are impulsiveness, hyperactivity, mental retardion, facial abnormalities, heart defects and motor problems.

• In FAS, many neurons receive less neurotrophins than usual and therefore undergo apoptosis.

• Children who are exposed to smoking before birth are at increased risk of aggressive behavior, attention-deficit disorder and impaired memory and intelligence (but smoking is not necessarely the reason, there is only correlation!).

• Immature neurons transplanted to new parts of the developing cortex develop characteristics of their new location. More mature neurons adopt some new properties while retaining some old ones.

• Our brains have an ability to remodel themselves as a response to our experinces. Axons and dendrites continue to modify their structure over the lifetime.

• The gain or loss of dendrite spines means a turnover of synapses, and it is probably linked to learning.

• Thickness of the cerebral cortex declines after approximately the 30th birthday, however both mental and especially physical activity enhance the activity of the brain, brain volume, and the thickness of the cortex.

• Losing a sense does not change the receptors of other sense organs, but it does increase attention to other senses.

• Different brain areas can change their functions to some degree, e.g. touch information can be processed by the occipital cortex in blind people.

• Practicing a skill (e.g. playing an instrument) reorganizes the brain to maximize performance of that skill.

• When compared to children playing some instrument the researchers noted that the sooner the child started playing, the more advantage they had on several tasks.

• Musicians have expanded representation of fingers on their cortex. However, extensive practicing can also lead to a condition where the representation of each finger overlaps with the representation of another finger. This is known as focal hand dystonia (or 'musician's cramp'').

Injuries of the Nervous system

Brain damage occurs for several several reasons: radiation, tumors, infections, toxic chemicals and degenerative conditions (e.g. Alzheimer's disease).

In young people the most common reasons are closed head injury and blood clots in the veins of the brain. In older people the most common reasons are strokes: 

1. In ischemia blood flow stops because of a clot in an artery, neurons are deprived of blood. This causes loss of oxygen and glucose.

2. In hemorrhage it is caused by a ruptured artery, neurons are flooded with blood. This causes excess of oxygen, calcium etc.

Both lead to same problems:

1. Edema, the accumulation of fluid.

2. Impairment of sodium-potassium pump (accumulation of sodium inside the cells).

Consequently, these combined problems lead to an excess of transmitter glutamate and overstimulation of neurons. This leads to an excess number of positive ions inside the cell. Ultimately the result is the death of neurons.

Nowadays the probability of survival after ischemia is good if it is treated quickly (< 3 hours) with tPA (tissue plasminogen activator). Prospects are not as positive for hemorrhage patients.

Methods of preventing brain damage after strokes:

1. Preventing overstimulation by blocking glutamate synapses.

2. Cooling the brain.

3. Use of cannabinoids.

4. Injections of omega-3 fatty acids.

After a stroke many surviving areas of the brain increase or reorganize their acitvity. They can compensate damaged areas in many ways.

Diaschisis is a sudden loss of function in an area of the brain connected to, but at a distance from a damaged area. Stimulant drugs can also be used for recovery. A whole destroyed cell can not recover, but damaged axons can grow back. Regeneration of the axon depends whether the neurons are located in the peripheral or the central nervous system. In CNS, axons regenerate only moderately and the injury is permanent.

Chapter 6 - Vision

A. Visual perception

Activation of a certain sensory nerve always conveys similar information to the brain, and therefore produces the same kind of reaction.

Information processing depends on three factors:

2. Which neurons are responding (e.g. pain).

3. The amount (amplitude) of response.

4. The timing of the response.

The law of specific nerve energies, first proposed by Johannes Müller, states that the nature of perception is defined by the pathway over which the sensory information is carried, the origin of the sensation is not important. For example, if you rub your eyes, the stimulus is perceived as visual even though it is actually the pressure on the eyes.

The visual system does not duplicate the image we see, as suggested before. Instead the visual system codes it in neuronal activity.

The pupil is the center of the eye that allows light to enter the retina (inner surface of the eye).

The cornea is a transparent part of the eye that covers the pupil. Together with the lens, the cornea refracts light.

The route of the information from retina to the brain is indirect: first it goes to bipolar cells near the center of the eye. The bipolar cells then pass it on to the ganglion cells directly or indirectly (via amacrine cells). The axons of the ganglion cells gather together and pass the information to the brain.

The blind spot is a region of the retina where the optic nerve and blood vessels pass through to connect to the back of the eye. There are no receptors.

The fovea is an area of the retina responsible for sharp central vison. It has a lot of receptors, each of these receptors are connected to a bipolar cell, and each of these bipolar cells are connected to a ganglion cell (more precisely, midget ganglion cell). Each receptor in the fovea has a straight path to the brain.

There are two kinds of visual receptors on the retina:

• Rods are plentiful in the periphery of the retina and they work better in dim light.

• Cones are plentiful in and around the fovea and they are responsible for color vision. They function best in relatively bright light.

The human eye has much more rods than cones (ratio is 20:1), however cones provide the majority of the input of the brain. This is because in the fovea, all the cells, i.e. cones, have a straight path to the brain.

Photopigments are chemicals in the rods and cones that deliver energy when affected by light.

There are three types of cone photoreceptors. These receptors are sensitive to different portions of the visible spectrum. For humans, the visible spectrum ranges approximately from 380 to 740 nm.

There are different theories related to color vision:

• The Trichromatic Theory.

• The Opponent-Process Theory.

• The Retinex Theory.

Pioneers of color vision are Thomas Young and Hermann von Helmholtz, who created the trichromatic theory of color vision, also known as Young-Helmholtz theory, which states that we perceive colors by comparing the responses of different kind of cones.

The response of a given cone varies not only with the wavelength of the light that hits it but also with its intensity, and the brain would not be able to discriminate different colors if it had input from only one type of cone. This is why interactions between at least two types of cone is necessary to produce the ability to perceive color.

Different cone types are short-wavelength, medium-wavelength and long-wavelength. Short-wavelength cones are scarcer than the two other types.

The opponent process theory is based on the idea that the visual system records the differences between the responses of cones; all the colors are perceived as continuums from yellow to blue, from red to green and from white to black. Negative color afterimage in optic illusions is an example of how this process works. It is also suggested that the bipolar cells can get fatigued after prolonged stimulation, which can cause alterations in our perception.

As the trichromatic theory and the opponent process theory could not explain color constancy (we recognize colors even when the lighting is changing), so the retinex theory was created. This theory states that both the eye and the brain are involved in the processing, and the information from different parts of retina is combined on the cortex.

People differ in the number of different types of cones they possess. That is, the people with only one or two kinds of cones have color vision deficiency (color blindness). Red-green color deficiency is the most common, as 8% of men and 1% of women have it. Some women also have one extra type of cone (4 in total), but it does not change their vision drastically.

B. Neural basis of visual system

Overall vision consists of different aspects which are processed on different parts of cortex.

All the optic nerves from both eyes meet at the optic chiasm, where approximately half of the axons lead to the other side of the brain.

Lateral inhibition refers to the inhibition that neighbouring neurons in brain pathways have on each other. The practical result is sharper contrasts.

The cells of the retina are on layers in the following order:

1. Photoreceptors (rods and cones) on the bottom.

2. Horizontal cells.

3. Bipolar cells.

4. Amacrine cells.

5. Ganglion cells which lead to the lateral geniculate nucleus on the thalamus.

The horizontal cells are local cells (no axons nor action potentials), which means that its depolarization decreases with distance. It is spread in such a way that it affects many bipolar cells.

Photoreceptors have naturally a certain level of activity, and light decreases their output. Because their synapses onto bipolar cells are inhibitory, light makes them decrease their inhibitory output.

One photoreceptor excites one bipolar cell, and it also excites a horizontal cell which instead inhibits the very same bipolar cell. The excitatory synapse in the bipolar cell is greater than the inhibition. However, as mentioned before, the spread out horizontal cell inhibits surrounding bipolar cells which do not receive excitation; this process causes lateral inhibition.

The area of the visual field from which light hits a receptor is called the receptive field of that receptor. For any cell in the visual system, the receptive field depends on which receptors are linked to that cell.

There are three kinds of primate ganglion cells:

• The parvocellular neurons (small cell bodies and receptive fields, located in fovea) are specialized in visual details and color vision.

• The koniocellular neurons (small cell bodies and receptive fields, located all over the retina) have several tasks.

• The magnocellular neurons (large cell bodies and receptive fields, located all over the retina) are specialized in moving stimuli and large patterns.

After the information reaches the lateral geniculate nucleus it goes to primary visual cortex (also called area V1 or striate cortex) in the occipital cortex, which is important for conscious visual perception.

A damage on V1 can lead to blindsight: a condition in which the person responds to visual stimuli without consciously perceiving them. Several explanations have been suggested, e.g. tiny islands of healthy tissue on V1 could produce the phenomenon, or other branches of the optic nerve convey visual information to the superior colliculus and other areas.

From the primary visual cortex the information goes to secondary visual cortex (area V2) which conveys it further after processing it. The connections in the visual cortex are reciprocal.

Different pathways within the cerebral cortex respond to different stimuli. The ventral streams are visual paths in the temporal cortex and their function is to identify and recognize objects. The dorsal streams are visual paths in the parietal cortex which help the motor system find and use objects.

The visual cortex consists of several types of cells:

• The simple cells are located in V1 with small, bar-shaped or edge-shaped receptive field. Fixed excitatory and inhibitory zones.

• The complex cells are located in V1 and V2 with average, bar-shaped or edge-shaped receptive field. No fixed excitatory or inhibitory zones.

• End-stopped cells (hypercomplex cells) are located in V1 and V2 with large, bar-shaped receptive field.

Similar cells are gathered together at the visual cortex in columns.

The neurons on the visual cortex are suggested to be feature detectors, responding to a particular feature (e.g. bars). Prolonged exposure to a certain feature decreases sensitivity to that feature. In a sense, the cell is fatigued.

The information processing gets more complex as the information goes further in the visual cortex. In the inferior temporal cortex it is rather complicated, that brain area takes care of the capacity of shape constancy (the ability to recognize the shape of an object even when its position or angle is changing).

Visual agnosia is an inability to recognize or interpret objects in the visual field. It is caused by damage in the temporal cortex.

In prosopagnosia the ability to recognize faces is impaired, while the ability to recognize other objects may be relatively intact. It is caused by damage in the fusiform gyrus.

Area V4 is essential for the perception of color constancy. It also affects visual attention.

Some areas, especially MT (also known as middle-temporal cortex, or V5) and MST (medial superior temporal cortex), are specialized in motion. Motion of an object is perceived relative to its background.

Saccades are quick, simultaneous movements of both eyes in the same direction. During saccades, several of the visual areas decrease their activity.

In motion blindness a person cannot perceive motion in his or her visual field, despite being able to see stationary objects without issue. Some Alzheimer patients also have a mild dysfunction of motion perception. The opposite condition is also possible, a person is blind but regardless is able to see the direction in which an object is moving. All these conditions display how different areas of the brain process different kinds of visual information.

C. Development of the visual system

The human cortex is the most plastic during the first years of the life.

Human infants start to focus on faces already during the first days of their lives. This supports the idea of an innate face recognition module.

The skills in face recognition develop until adolescence. How precise the recognition is depends on the exposure to certain face characters. This is based on the process in the inferior temporal cortex: it defines the 'average face', which all faces are then compared to.

The development and fine-tuning of the brain requires visual experiences. It is important for the neurons of the visual cortex to receive binocular input (signals from both eyes).

Axons from the eyes fight for responsiveness with each other. If the one eye is closed, the other one will outcompete its synapses, which can lead to a condition called 'lazy eye'. However, if both eyes remain closed for some reason, then the person will not become blind.

The 'lazy eye' can be treated by covering the active eye. This method will not enhance stereoscopic depth perception, but it will activate the dysfunctional eye. Other treatment is to ask a child to play a video game with three-dimensional display. Fun and beneficial for the stereoscopic depth perception at the same time!

Stereoscopic depth perception is obtained by comparing the different inputs from the eyes. This happens because the brain detects retinal disparity. This will not happen if the eyes can not work at the same time.

During sensitive periods, experiences have a very strong influence. Different aspects of vision have different sensitive periods. After the sensitive period the visual cortex will not change much. E.g. those who are not exposed to moving stimuli early in life will become motion blind.

Inhibition by GABA starts the sensitive period, and researchers are hopeful they could relaunch the sensitive period by blocking GABA receptors.

Astigmatism is an optical defect in which vision is blurred due to the inability of the optics of the eye to focus a point object into a sharp focused image on the retina. Approximately 70% of infants have this condition, though its prevalence diminishes significantly with age.

A cataract is a clouding of the lens in the eye. The sooner the visual impairments are fixed, the better the recovery, though some subtle visual deficits remain.

Chapter 7 - The other sensory systems

A. Audition

Physically sound waves are compressions of air, water etc.

The amplitude of a wave refers to its intensity. Loudness differs from amplitude.

The frequency refers to the number of compressions per second (in hertz, Hz). The human ear can detect sounds within the range 15-20,000 Hz. The higher the frequency, the higher the pitch.

Structures of the ear fall into three categories:

• The outer ear, which consists of the pinna (helps to locate the source of a sound).

• The middle ear, which contains the tympanic membrane (the eardrum) which vibrates the sound to three bones (hammer, anvil and stirrup).

• The inner ear, which contains the oval window and the cochlea.

There are different theories about how we actually differentiate between sounds:

1. Place theory is a theory which states that our perception of sound depends on where each component frequency produces vibrations along the basilar membrane.

2. Frequency theory states that the basilar membrane synchronized with a sound so that the nerve axon produces action potentials of the same frequency.

3. Current perspective contains some parts of both of these theories:Volley principle attempts to account for the maximum theoretical limit for the neuronal firing of action potentials and the small time scales over which sound discrimination must occur. Auditory cells time their responses very precisely.

Most of our hearing occurs under 4000 Hz.

People differ in sensitivity to pitch. Amusia refers to an impaired ability to detect frequency changes.

Amusia has a genetic base and it is caused by weak connections between the auditory cortex and other brain areas.

Absolute pitch refers to ability to recognize a note. Most people are either very accurate or not accurate at all; extensive musical training is important. Speakers of tonal languages have more often absolute pitch.

Auditory information is processed on the primary auditory cortex A1 (a part of the superior temporal cortex). Also audition has a 'what' pathway and a 'where' pathway, the first one being sensitive to patterns of sounds and the second one to sound location. Therefore it is possible to be motion deaf.

The development of the auditory system requires experience.

A damage on the primary auditory cortex does not lead to deafness. Instead, the auditory cortex offers a “map' of the sound (tonotopic map), and therefore damage can lead to impairments in processing auditory information.

The cells in the auditory cortex are more responsive to one kind of preferred sound.

There are also other auditory areas in the brain, but they process sounds from different perspective.

Two types of hearing impairments have been distinguished:

• Conductive deafness (also middle-ear deafness) is caused by e.g. tumours or diseases

• Nerve deafness is caused by a damage in the cochlea, the hair cells or the auditory nerve.

Some prenatal conditions can result in nerve deafness, e.g. lack of oxygen during birth, exposure to certain drugs, and exposure to diseases such as syphilis or meningitis. Nerve deafness can also be inherited.

With two ears we can localize the source of a sound. One cue is the difference in intensity between the ears. The second cue is that sound waves arrive at the ears in different times. The third cue is the phase difference which is used with low frequencies, loudness differences are used with high frequencies.

B. The Mechanical Senses

The mechanical senses detect mechanical stimuli, e.g. touch, pain and balance. Also audition is a mechanical sense because the hair cells are a form of touch receptors.

The vestibular system is a sensory system that provides the leading contribution about movement and sense of balance. The vestibular organ function is to detect the direction of tilt and the acceleration of the head.

The vestibular organ consists of the saccule, utricle and three semicircular canals. The hair cells are located in those semicircular canals and next to the hair cells lie particles called otoliths. Otoliths move different hair cells when the head tilts in some direction.

The somatosensory system refers to the movements and sensations of the body. It includes different senses including pressure, cold, warmth, pain, tickle, itch, discriminative touch and the position and movement of joints.

Most of the receptors respond to different kinds of stimuli, e.g. to pain, warmth and cold.

A touch receptor can be a bare neuron ending, an elaborated neuron ending or a bare ending surrounded by other cells that affects its functioning.

Pacinian corpuscles are one of the four major types of mechanoreceptor. They are nerve endings in the skin, responsible for sensitivity to vibration and pressure.

Besides the changes in temperature, also certain chemicals can induce the feeling of coolness or warmth. Capsaicin is a chemical which stimulates the heat receptors. Menthol and mint cause a feeling of coolness.

Information from touch receptors is gathered through the cranial nerves (head) and through the spinal nerves (other parts of the body). Every spinal nerve has a sensory component and a motor component. Each spinal nerve also innervates (supplies with nerves) a certain area, a dermatome. These dermatomes overlap with each other.

Different kinds of sensory information have different pathways into the brain. Therefore the aspects of body sensations stay apart on the way to the cortex. For the conscious experiences of touch, the primary somatosensory cortex is the key player.

The experience is not necessarily the same as the stimulus, e.g. you can feel two touches nearby each other as one somewhere in between those touches.

The perception of the body can become distorted as a result of damage to the somatosensory cortex.

Pain receptors are bare nerve endings, and they can respond to pressure, acids and heat. The axons of the pain receptors have only a little myelin and therefore their conductance is not very quick; however, the brain processes pain information quickly.

The axons conducting pain information release two transmitters:

• Glutamate which is released after mild pain.

• Substance P which is released after severe injury together with glutamate.

Pain information has two pathways to the brain:

• To the somatosensory cortex, where the sensory information is led.

• To the cingulate cortex, which is responsible for the emotional feeling of pain (e.g. 'sympathetic pain').

The function of the pain is to alert from the danger threatening the tissue. Therefore it is dangerous not to feel pain.

Continuing pain is decreased by opioid mechanisms, which work by blocking the release of substance P.

The body also has its own opiate-type chemicals, called endorphins. Endorphins are released as a response to pain, but also during sexual intercourse or listening to music.

A placebo is a fake medicine, which can cause actual effects, e.g. they can relieve pain. This happens, however, through mental processes: a placebo decreases the functioning of the cingulate cortex but not the somatosensory cortex. In a chemical level the function of placebos is partly based on the release of opiates.

A nocebo is an antiplacebo, which can increase pain by causing anxiety.

Cannabinoids and capsaicin can be used to relieve pain. Also electrical stimulation of the spinal cord or the thalamus can be effective, though most of the patients do not report long-lasting pain reduction.

As the body has mechanisms to reduce pain, it has also mechanisms to induce it. Damaged skin releases chemicals (e.g. histamin) which help recovery but at the same time stimulate pain receptors nearby.

Anti-inflammatory drugs (e.g. ibuprofen) works by reducing the release of those chemicals.

Synaptic receptors can 'strengthen', so that similar input in the future causes a stronger response. This kind of mechanism is essential for learning, but is a burden when it comes to painful stimuli.

In the past, itch was considered as a form of pain, nowadays they are separated from each other. The relationship between pain and itch is inhibitory (e.g. opiates decrease pain but increase itch).

One spinal pathway is responsible for itch, and the response is rather slow. Itch causes a release of a chemical called gastring-releasing peptide.

C. Taste and Olfaction

A sensory system can use two types of coding:

• Labeled-line principle, in which the receptors respond to certain stimuli and the meaning depends on which neurons are active.

• Across-fiber pattern principle, in which receptors respond to many stimuli and the meaning depends on the relationship of neurons.

Taste buds contain taste receptors on the tongue (on the papillae), and actually they are modified skin cells. Taste receptors are also replaced rather often, like skin cells.

Flavour refers to a combination of taste and smell. Both taste and smell axons are connected to the endopiriform cortex.

Traditionally four primary tastes have been separated: sweet, salty, sour and bitter. Also a fifth has been suggested: glutamate (umami).

Adaptation refers to the fatigue of the receptor after exposure to a certain taste. Cross-adaptation means weaker response to one taste after exposure to another.

Different substances excite different receptors and strike different sequences of action potentials.

A receptor which responds to salty taste detects sodium. Sour receptor detect acids. Sweetness, bitterness and umami are similar to each others chemically. Bitter substances are usually somewhat toxic.

Taste information from the tongue goes along the seventh, ninth and tenth cranial nerves. These nerves project to the nucleus of the tractus solitarius. From there the message shatters to several brain areas.

Individual differences in tasting are huge. Some people are non-tasters, as some are the other extreme: supertasters. Supertasters are prone to avoiding strong-tasting foods. Taste sensitivity is linked to the number of fusiform papillae on the tongue.

Olfaction refers to the sense of smell. Membranes inside the nose respond to chemicals.

Olfaction is important for most of the mammals, though it is not that important to humans anymore. However, it can be improved a lot with practice.

Olfactions function is to detect eatable foods. It plays a part also in social settings: when people are asked who they would prefer as a potential partner they prefer people who smell similar to themselves (but not too similar!).

It is estimated that humans have several hundred olfactory receptor proteins. The amount is so huge because olfaction does not work as a single continuum.

Olfaction adapts quickly. It is faster than researchers once believed.

The message from an olfactory receptor goes to the olfactory bulb, and from there to the olfactory area on the cerebral cortex.

Experience can teach us to differentiate better between similar smells.

Olfactory receptors are rather vulnerable to damage.

Women are more sensitive to smells than men. We don't yet know much about genetic variations when it comes to olfactory, but there are significant differences.

Receptors in the vomeronasal organ (VNO) are specialized to detect pheromones. Pheromones are chemicals which have an especially sexual impact on other humans/animals. VNO receptors do not adapt as olfactory receptors adapt. However in humans VNO is small and has no receptors, but we have some other receptor resembling those in VNO. Probably pheromones affect our behaviour unconsciously.

Women who spend a lot of time together synchronize their menstrual cycles. In sum, body secretions work as pheromones and affect us in subtle ways.

Synesthesia is a condition in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second sensory or cognitive pathway. For example a smell can be perceived as a color.

Chapter 8 – Movement

A. The control of movement

Muscle contractions produce movements.

Three different kinds of muscles are distinguished:

• Smooth muscles: inner organs. Cells are long and thin.

• Skeletal (striated) muscles: movements of the body. Cells are striped and long.

• Cardiac muscles: heart contractions. Cells are connected to each others, and therefore they all contract at once.

Fibers form muscles. Each muscle receives information from only one axon, but one axon can innervate several muscles. 

A synapse between a motor neuron axon and a muscle fiber is called a neuromuscular junction. Acetylcholine is a neurotransmitter that is released in the junction and it makes the muscle contract.

Most muscles work in pairs, as flexor and extensor muscles. These opposing sets of muscles are called antagonistic muscles.

Myasthenia gravis is a disease characterized by fatigue of skeletal muscles. The cause is the impairment in acetylcholine receptors.

We have two kinds of muscle types:

• Fast-twitch fibers, which are anaerobic, get easily tired. On the other hand the contraction is fast.

• Slow-twitch fibers, which are aerobic, do not fatigue easily. The contraction is strenuous.

Individuals differ in the number of fast-twitch fibers and slow-twitch fibers.

Proprioception is the sense of the relative position of neighbouring parts of the body. A proprioceptor is a receptor of this sense, they detect the tension and stretch of a muscle. When the muscles is stretched, a reflex will contract it as well - this is called a stretch reflex.

A muscle spindle is sort of a proprioceptor. Another type is a golgi tendon organ, which detects the variations in muscle tension. It works as a brake; if the tension is too much they inhibit further contraction.

A reflex is an automatic response to a stimulus, e.g. pupil changes when light hits it.

Infants have some reflexes adults do not have:

• Grasp reflex, an infant grasps an object which is placed in his/her hand.

• Babinski reflex, extension of the big toe when touching the sole of the foot.

• Rooting reflex, an infant turns his/her head when the cheek is being touched.

Most of the movement consists of voluntary and involuntary movements.

Movements vary in how they respond to feedback. Ballistic movements do not correct themselves.

Some actions are quick sequences, such as speaking, writing etc. A central pattern generator is a neural mechanism generating rhythmic patterns.

Built-in movements occurring in a fixed sequence are called motor programs (e.g. yawning).

B. Neural Basis of Movement

The primary motor cortex is important in eliciting movements, especially intended movements. The motor cortex innervates muscles via the brainstem and spinal cord.

There are several areas important for moving near the primary motor cortex:

• The posterior parietal cortex detects the body’s position in relation to the surrounding world.

• The primary somatosensory cortex processes sensory information, e.g. touch.

• The prefrontal cortex detects lights, sounds and other signals affecting to movement. Furthermore, it considers the probable outcomes of movements.

• The premotor cortex participates in preparing a movement.

• The supplementary motor cortex plans and organizes sequences of movements.

Mirror neurons are neurons which activate while preparing for the action and while watching someone else performing. This is interesting, because mirror neurons can be important for understanding other people, identifying with them and learning from them.

Still it is not clear whether mirror neurons cause imitations or if they are developed by the imitation. At least some of them develop their mirror qualities.

It is suggested that dysfunctional mirror neurons are part of autistic disorder.

Before an activity, the motor cortex produces a readiness potential - the brain activity for the movement starts before a conscious decision.

The previous fact does not mean we do involuntary movements, but that our voluntary movement is unconscious in the beginning.

The corticospinal tracts are paths from the cerebral cortex to the spinal cord. We have two of those tracts:

• The lateral corticospinal tract control movements in peripheral areas. Axons of this tract connect directly to their target neurons.

• The medial corticospinal tract control movements of the neck, shoulders and trunk, and therefore it is related to walking, sitting, turning etc.

Both paths cross in the medulla.

Several disorders in the spinal cord can affect the control of movements (e.g. paralysis, paraplegia, and poliomyelitis).

The cerebellum is an important area for balance and coordination. Damage to that area produces clumsiness, speaking problems, and inaccurate eye movements. The individual has problems with activities requiring timing and aiming.

However, the cerebellum also responds to sensory stimulation without movements.

The cerebellum affects also affects attention: people with cerebellar damage require more time when they have to shift their attention.

The information from the cerebellum goes to the cerebellar cortex. The neurons on the cerebellar cortex have a geometrical pattern. The Purkinje cells and the parallel fibers are located on the cerebellar cortex.

The basal ganglia refers to a group of subcortical structures in the forebrain, such as the caudate nucleus, the putamen and the globus pallidus.

The caudate nucleus and putamen controls which movements to stop inhibiting. The basal ganglia is important for initiating an action and learning new habits.

All the brain areas are important for learning new skills, and the neurons in the motor cortex adjust their activity.

C. Movement and Diseases

Parkinson's disease is characterized by slow movements, shaking, rigidity, and difficulties in mental and physical activities. Many patients are also depressed and have impairments in memory and reasoning.

In the age class +65 years approximately 1-2% have the disease.

Researches have been curious about what determines the speed of movements. According to one hypothesis we balance between speed and accuracy. The symptoms of Parkinson's disease does not support this theory.

In Parkinson's disease many neurons die, especially in the substantia nigra. This causes the lack of dopamine, which causes excessive inhibition of the thalamus and decreased excitation of the cerebral cortex.

Normally people lose about 1% of the neurons in substantia nigra per year after the age of 45. Impairment of 20-30% neurons start Parkinson's disease symptoms. However, individual differences are huge again, and the disease can have early-onset or late-onset.

In the cell level the damage in Parkinson's disease takes place in the mitochondria.

Heritability of Parkinson's disease is low. The effect of genes is greater in early-condition Parkinson's disease.

Some toxins can destroy cells in the substantia nigra and therefore increase the risk of Parkinson's disease. For example herbicides and pesticides are known to cause the disease.

L-dopa (a precursor of dopamine) is the most common treatment for Parkinson's disease. Dopamine itself is not efficient because it would not pass the blood-brain barrier. However, L-dopa does not work for every patient, it does not stop the neurons dying, and it has some nasty side effects (e.g. nausea, sleeping problems and hallucinations).

Also other treatments are suggested, e.g. neurotrophins, antioxidants, dopamine receptor stimulants, electrical stimulation in certain brain areas, apoptosis decreasing drugs etc.

Also brain transplants are one option, but so far they have not worked in practice.

Huntington's disease is a disease that affects muscle coordination and leads to cognitive decline and dementia. Usually it starts with tremors, which later start to affect walking, speech etc.

Also psychological symptoms are present: depression, drug abuse, alcoholism, sexual problems, sleep disorders and anxiety. Sometimes psychological symptoms start before physiological and therefore the patient can be misdiagnosed.

Usually Huntington's disease starts at the age 30-50. However, the disease is relatively rare.

Huntington's disease is characterized by brain impairments in the caudate nucleus, putamen, and globus pallidus.

Researchers have found a gene related to Huntington's disease. A sequence of bases C-A-G (cytosine, adenine, and guanine) determines the likelihood of the disease, as well when it might strike. People with more repeats of those bases have an earlier onset.

Everyone has a protein huntingtin which is essential, but its mutant form causes Huntington's disease when occurring in the brain.

Several treatments are suggested, e.g. neurotrophins, tetrabenazine, and sleeping pills.

Chapter 9 - Sleep

Rhythms of Sleep

The body has an innate rhythm of sleep and wakefulness. This rhythm is self-generated.

Endogenous circannual rhythm refers to innate rhythm for seasonal changes.

Endogenous circadian rhythm refers to innate rhythm that lasts approximately a day. The rhythm can be altered moderately, but major abnormalities from the 24-hour norm do not work out.

People vary in their circadian rhythms (morning people/evening people). Circadian rhythm also changes as a part of aging; children prefer to go to bed early, adolescents later, and at the age of 20 people start to feel sleepy earlier and earlier.

Free-running rhythm refers to a rhythm which is not interfered by any stimulus.

The circadian rhythm is reset by zeitgebers ('time-giver' in German). Light is the major zeitgeber, as also noise, meals, temperature and exercise function as zeitgebers.

Blind people either adopt free-running rhythm or set their rhythm to stimuli other than light.

Jet lag is a condition which results from alterations to the body's circadian rhythm; circadian rhythm is either phase-delayed or phase-advanced. Jet lag results from rapid crossing of time zones, and the symptoms can vary from sleepiness to depression and problems in concentration. Jet lag causes greater stress to some people than to others. During stress a hormone called cortisol is secreted, and in a long run it can result in impairments in the brain and memory. Adjusting to night shifts is rather difficult for many people. Those people working at nights have more accidents than day-shift workers. Circadian rhythm is a robust mechanism, which is not easily changed.

The suprachiasmatic nucleus (SCN) is responsible for setting the circadian rhythm. This process happens naturally by genetical control.

The SCN is located above the optic chiasm. The pathway from retina to SCN is called retinohypothalamic path. The retinal ganglion cells on that path have their own photopigment, melanopsin.

The biochemical basis of the biological clock:

1. Genes called period and timeless produce proteins called per and tim.

2. Light increases the production of per and tim, which increase the activity of the suprachiasmatic nucleus.

3. Gene mutations in period and timeless can make the circadian rhythm longer or shorter.

The superchiasmatic nucleus regulates several brain areas, for example the pineal gland. The pineal gland is an endocrine gland releasing the hormone melatonin, which controls circannual and circadian rhythms. Melatonin is secreted during night. Melatonin pills are used as sleeping pills.

Stages of sleep and brain activities

Coma is a state of unconsciousness, in which a person cannot be awakened and fails to respond normally to any stimuli. It is caused by stroke, disease or damage in the head.

A person in a vegetative state shows partial arousal instead of true awareness, without purposeful activities. A person in a minimally conscious state can have moderate purposeful activities. Both states can last for months or even years.

Brain death is a condition in which all the brain activity ends.

Polysomnography is a method combining EEG and eye-movement recording.

Stages of sleep:

Stage 1: irregular, low-voltage waves. Brain activity is less than during wakefulness.

Stage 2: K-complexes (high-amplitude waves) and sleep spindles (12-14Hz waves in a burst).

Stages 3 & 4: slow-wave sleep (SWS), large-amplitude waves.

Stage 5: rapid eye movement (REM) sleep or paradoxical sleep. Increased brain activity, relaxation of muscles, irregular heart rate and breathing.

Stages 1-4 are also known as NREM sleep (non-REM).

Dreams are usually seen during REM sleep, but also in other sleep stages.

The sleeping process goes through stages 1-4, then back to 3 and 2 and then to REM. This cycle lasts about 90 minutes and is repeated again. REM sleep is most common in the morning.

The midbrain is an essential structure for maintaining wakefulness. Also pontomesencephalon (part of the reticular formation) is important for cortical arousal. The locus coeruleus improves the recollection of recent memories and increase wakefulness. It stays inactive during sleep. Activation of the pons precedes the REM phase.

The pons originates PGO waves (pons-geniculate-occipital) during REM sleep, and it also relaxes large muscles.

Interaction between neurotransmitters serotonin and acetylcholine is essential for REM sleep.

One of the pathways of the hypothalamus releases neurotransmitter histamine. It has excitatory influences, so it is released during arousal.

Another pathway from hypothalamus releases neurotransmitter orexin (aka hypocretin). It is essential for maintaining wakefulness.

Some of the axons from the basal forebrain release acetylcholine which also increases arousal.

GABA is essential for sleep, as it inhibits synapses.

Most adults need approximately 8 hours of sleep per night. However, individual differences are huge.

Insomnia refers to sleeping difficulties. Insomnia is caused by several reasons including noise, too hot or cold environment, pain, stress, mental disorders, medications etc.

Prolonged use of tranquilizers or alcohol can also cause insomnia, since the person is not able to fall asleep without those substances.

Sleep apnea is a type of insomnia which is characterized by interruptions in breathing while sleeping. As a consequence the sleep is disjointed, people suffering from sleep apnea experience sleepiness, depression, brain impairments etc.

Hormones, genetics and obesity affect sleep apnea. Patients are told to lose weight and avoid alcohol and tranquilizers.

Narcolepsy is a cronic sleep disorder characterized by excessive daytime sleepiness. Other symptons are cataplexy (sudden muscle weakness), hypnagogic hallucinations (dreamlike hallucinations which can be difficult to identify as dreams) and sleep paralysis (inability to move during sleep). Narcolepsy is related to lack of neurotransmitter orexin.

Night terror refers to experiences of extreme terror and anxiety durin NREM sleep. It is more common in children than adults.

Talking while sleeping is common among people in any age, while sleepwalking is more common among children. Sleepwalking can be dangerous, but it is not dangerous to wake up a person who is sleepwalking. Sexsomnia is a condition in which person either masturbates or has sex with her or his partner while sleeping.

Functions of Sleeping

While sleeping, the body rests its muscles, rebuilds proteins, reorganize synapses and decreases metabolism. For these reasons sleep is essential for us. All species sleep.

Hibernating animals save energy while food is scarce. Hibernation slows the aging process significantly.

Animals differ in their sleeping patterns, for example dolphins sleep with only one brain hemisphere. Required sleeping hours vary as well.

Because GABA is released during night, sleep deprivation leads to an accumulation of GABA. Sleep deprived individuals are more prone to accidents and show weakened performance.

People who suffer from sleep deprivation the least are usually 'evening people', who have higher levels of brain arousal.

Caffeine is a chemical which works against adenosine and increases arousal.

Sleep enhances memory. It also helps to reanalyze memories. Practically the same processes in the brain are repeated during sleep, so the experiences are reinforced. On the other hand, other connections are also weakened.

Sleep spindles are related to learning, as they indicate the information exchange between the thalamus and cerebral cortex. Learning increases sleep spindles, and there is high correlation between nonverbal IQ test results and the amount of sleep spindles.

The more hours of sleep in total, the higher the percentage of REM sleep. The length of NREM varies less.

NREM sleep is more related to verbal learning, and REM sleep to learning of motor skills.

MAO inhibitors (used as antidepressants) decrease REM sleep. However, they do not seem to impair memory.

According to one theory, eye movements during REM increase the oxygen supply to the cornea. The truth about the function of REM sleep still stays unknown.

Different hypotheses on the function of dreaming:

1. Activation-synthesis hypothesis: the function is to organize information.

2. Clinico-anatomical hypothesis: the main sources of dreams are motivations and memories, but also external inputs play a part.

Chapter 10 – Internal regulation

Temperature

Several studies on animals and humans indicate the necessity of temperature for behavior, learning, development etc.

Homeostasis refers to biological processes which keep the body in a stable, constant condition. The body has a range within values have to fit, usually this range is so narrow that it is also called a set point. For example blood levels of oxygen, glucose, sodium chloride, protein, fat and acidity need to be stable.

Set points can have seasonal changes, for example many animals increase their body fat before cold winter. The term allostasis refers to this adaptive mechanism the body uses to change its set points.

Negative feedback is a process that reduces alterations from the set point.

Maintenance of homeostasis (basal metabolism) consumes a lot of energy: approximately 2/3 of total energy consumption.

If an animal is poikilothermic, its internal temperature varies considerably. It is the opposite of a homeothermic animal which maintains thermal homeostasis. Humans, as most of the other mammals, are homeothermic, we generate heat in respect to our total mass and radiate in respect to our surface area.

We have two kinds of mechanisms to control body temperature:

1. Behavioral: putting more clothes or taking them off, cuddling with other people or animals or other warm objects, increasing or decreasing activity.

2. Physiological: when hot, we sweat. (Other animal can also pant or lick themselves). When cold, we shiver, decreasing blood flow in the skin.

The advantage of being homeothermic is that we are able to be active even when the weather is cold.

The brain areas which are related to the control of body temperatures are in and around hypothalamus. These areas are called preoptic area/anterior hypothalamus (or POA/AH). If these areas are cold an animal acts like the environment is cold even though it was warm.

Fever is the immune systems mechanism to slow down the growth of bacteria and enhance its own activity. Leukocytes (white blood cells) of the immune system release cytokines which activate the hypothalamus to release prostaglandins. Prostaglandins are essential for fever.

In fever the set point changes. If the fever is too high, it can also be dangerous: 41°C is life-threatening. In that temperature proteins start to shatter.

Reproductive cells need a slightly cooler environment than the normal 37°C: this is the reason why men have testicles.

Thirst

70% of our body is water.

In the case of dehydration the body has several autonomic responses to control its homeostasis, e.g. producing more concentrated urine, decreasing sweating etc.

Vasopressin (also antidiuretic hormone or ADH) and angiotensin II are hormones which constrict the blood vessels and thus increase blood pressure.

Two types of thirst are:

1. Osmotic thirst, which is caused by changed concentrations.

2. Hypovolemic thirst, (referring to low volume) which is caused by the loss of water (e.g. excessive bleeding or sweating).

Osmotic pressure is caused by differences in the concentration inside and outside the membrane. A semipermeable membrane allows water to pass freely but not solutes. After eating something salty, sodium ions will increase in the extracellular fluid but not in the intracellular fluid. This condition draws water into the extracellular fluid and causes osmotic thirst.

Brain areas that detect osmotic pressure are OVLT (organum vasculosum laminae terminalis) and SFO (subfornical organ). The stomach has also some receptors for detecting sodium levels. These different areas are connected to parts (e.g. supraoptic nucleus and paraventricular nucleus) which control the release of vasopressin.

The digestive system has detectors which prevent overdrinking.

Sodium-specific hunger is caused by the lack of salt. It is increased by angiotensin II.

Hunger

Animals have different eating habits. Some eat a lot occasionally, some only what they need at the time. Habits of humans are somewhere inbetween the extremes.

The digestive system works to break the food down into a form that cells can use.

The enzymes in the mouth start to break down carbohydrates, food goes to the esophagus and stomach where the enzymes in the stomach start to break down proteins, then food goes to the small intestine where the enzymes break carbohydrates, proteins and fats.

Lactase is an enzyme breaking lactose (milk sugar). Some populations have the enzyme and some do not: for example it is more common in Scandinavia than Asia. Lack of the enzyme causes stomach cramps and gases when dairy products are used.

Carnivores (meat eaters) get all the nutrients rather easily. Herbivores (plant eaters) and omnivores (meat and plant eaters) have to plan their diets more precisely.

Not all food is eatable. We have several mechanisms to detect eatable food, such as taste receptors, learning from experience, and from others.

We start to like tastes more when we try them multiple times.

Conditioned taste aversion is a phenomenon which occurs when a taste is linked to illness: we start to dislike it.

Eating is not only fulfilling the biological needs, most of the people also like to eat and chew. However, a taste alone does not always leave an individual satisfied.

Stomach distention is the signal which stops us eating. The vagus nerve sends information about the stretching of the stomach walls and the splanchnic nerves sends information about nutrients.

Also signals from the duodenum (part of small intestine) report about the satiety. Food in the duodenum causes secretion of cholecystokinin (CCK) which closes the sphincter muscle between the stomach and the duodenum and stimulates the vagus nerve.

Glucose is the main source of energy. Glucose level stays quite stable over times because of the bodys control mechanisms.

Two pancreatic hormones regulate glucose level:

1. Insulin, which helps glucose to enter the cells.

2. Glucagons, which activates the liver to convert its glycogen into glucose.

If the insulin level is constantly high or low, a person increases eating. Low insulin level (as people with diabetes) causes the condition in which cells do not get glucose. A high level of insulin causes the opposite condition in which the glucose is pumped into the cell rapidly and blood glucose level remains low.

Insulin is an example of short-term regulation.

A chemical called leptin is responsible for long-term regulation. It is produced by fat cells. A high leptin level causes overall activation, increases the activation of the immune system and decreases hunger.

Leptin also triggers the puberty in the adolescence.

Usually overweight people have already high leptin levels, so leptin does not work as a drug if they want to lose weight. It seems like overweight people are less sensitive to leptin than some other people.

The arcuate nucleus of the hypothalamus is an essential area for controlling appetite. It has neurons which are sensitive to hunger information and neurons which respond to satiety.

The neurons responding to hunger receive information from the taste pathway and from axons releasing neurotransmitter ghrelin.

The neurons responding to satiety respond both to short-term and long-term regulation systems.

The paraventricular nucleus is an important area for the feeling of satiety. Receptors in the paraventricular nucleus (melanocortin receptors) send signals when it is time to stop eating.

Transmitters neuropeptide Y and agouti-related peptide block the satiety actions of the paraventricular nucleus and can cause overeating.

Also orexin (familiar from narcolepsy) is a chemical which controls appetite.

The lateral hypothalamus has several roles in eating. It controls insulin secretion by stimulating the pituitary gland, alters taste responsiveness and controls autonomic responses (e.g. secreting digestive enzymes).

Ventromedial hypothalamic syndrome is caused by a damage to the ventromedial hypothalamus. It leads to overeating and weight gain. A person with this kind of syndrome eats normal-size meals, but more often (because their stomachs empty faster than normal and an increase in insulin production).

Obesity is a severe problem in Western societies. Social, psychological and physiological factors are all to blame. Some mutated genes affect obesity. For example, melanocortin receptor can be impaired. Syndromal obesity refers to a state in which obesity is caused by a syndrome or other medical condition. Environmental factors also make a difference. Working life has changed, sedentary work is common nowadays. In the US, obesity is classified as a disease.

The best treatment for obesity is a change of lifestyle: more exercise, less food (or, better quality food). However, most people find it difficult to maintain a reduction in weight.

In general people who drink soft drinks are more obese. Soft drinks contain fructose which does not increase insulin level and therefore does not give the feeling of satiety. Diet soft drinks can cause obesity even more than normal soft drinks. Also drugs are used in the fight against obesity. For example fenfluramine, phentermine and sibutramine are commonly used. In extreme cases of obesity surgery can be used. Decreasing stomach size is the most common method.

In anorexia nervosa, an individual refuses to eat. Usually the disease strikes at adolescence. The mechanism behind anorexia is psychological; the person fears becoming fat. The triggers of anorexia are not well understood.

Bulimia nervosa is a disease in which the individual engages both in overeating and extreme dieting. Most bulimic sufferers also have another psychiatric disorder.

Some bulimics vomit after eating, trying not to gain weight.

Bulimia has been compared to drug addiction.

Chapter 11 - Reproductive behavior

Sex and Hormones

Steroid hormones are derivatives of cholesterol. They have several effects:

1. Cause rapid effects by binding to the membrane.

2. Activate certain proteins.

3. Either activate or inactivate certain genes by binding to chromosomes.

The sex hormones are also steroids, and they can be divided into three categories:

1. Androgens, or so called male hormones. E.g. testosterone.

2. Estrogens, so called female hormones.

3. Progesterone, also a female hormone. Secreted during pregnancy.

Sex-limited genes control the differences between men and women. In the brain they control apoptosis, making some areas larger in other sex.

The sex hormones have two kinds of effects:

1. Organizing effects, which influence whether the body will develop male or female characteristics: they take place before birth.

2. Activating effects, which refer to temporary activations caused by a hormone: can take place any time.

Genes cause a cycle of positive feedback, which causes the primitive gonads to develop into testes or ovaries.

Wollfian ducts are precursors for other male reproductive structures, and Müllerian ducts for female reproductive structures. Both men and women have a set of both ducts.

The Y chromosome (men have it) contains the SRY gene, which determines the development of testes. Because women lack in this gene, their gonads develop into ovaries.

The sensitive period is a time when hormones have strong, long-lasting effects. A high level of testosterone is linked to masculine development, a low level to feminine development.

Some drugs are prone to feminize development. Such drugs include alcohol, cocaine and marijuana.

Sex hormones also affect the hypothalamus, amygdala and some other brain areas. The sexually dimorphic nucleus is a part of the hypothalamus which controls sexual behaviors in men.

On the hypothalamus, testosterone works as an organizer. Sex hormones influence behaviors temporarily. Behaviors, in turn, also influence hormonal secretion. However, while hormones do not cause sexual behaviors, they still activate them by enhancing sensations. Sex hormones prime certain brain areas (e.g. the medical preoptic area, MPOA) to release dopamine. Dopamine increases sexual activity, as serotonin decreases it. Decreased sex hormone levels can result in memory impairments. Even though low testosterone levels on men decrease sexual interest, it does not cause impotence.

The menstrual cycle of women lasts approximately 28 days, and it is produced by the ovaries, hypothalamus and pituitary gland. At the end of the mestrual cycle, follicle-stimulating hormone (FSH) is secreted. It influences the growth of a follicle in the ovary. Together with luteinizing hormone (LH) FSH cause the release of the follicle.

Birth-control pills are used to prevent pregnancy by interfering with the normal feedback cycle of the ovaries and pituitary gland. Usually birth-control pills are combination pills containing estrogen and progesterone.

Women during the periovulatory period (the middle of the menstrual cycle) are more sexually active. They also find more masculine men more attractive.

Oxytocin is a hormone secreted by the pituitary gland. It is responsible for the contractions of the uterus during labor and the milk release from the mammary gland. It is also possibly important for the bonding between mating partners and a mother and her child.

Parenthood changes both the secretion of hormones and the pattern of hormone receptors. Hormonal changes help mothers to focus on their babies. Nevertheless, hormones are not necessary for parental behavior (adoptions!). Vasopressin is an important hormone for the bond between partners. It increases the commitment to the parenthood.

Variations in Sexual Behavior

Most people are not aware of how much diversity exists in sexual behaviors.

When it comes to animals, many sex differences have a function in terms of evolution. Evolutionary psychologists have suggested several differences among humans.

According to these theories, men can succeed by using either of two strategies:

1. Concentrating on one woman and offering her resources.

2. Mating with many women, when some of them might be able to raise their children without mans resources.

However, women can only become pregnant rather seldom, so for them it is better to focus on the quality rather than the quantity of mates. This explanation is one possible reason for mens desire for many sexual partners. On the other hand, women can also benefit from several partners: other men can offer better resources or children if her husband is infertile. Both men and women value intelligence, honesty and attractivity in a potential partner. Additionally women value wealth, success and good smell. The latter is explained by women smelling their potential mates immune systems - it should not be too similar. In many societies men have a preference for a younger partner. Possibly the explanation is that younger women have a longer period of fertitlity.

According to one hypothesis, men are more jealous of womens sexual infedility, and women are more jealous of mans emotional infedility. From the evolutionary perspective this seems plausible, but studies have suggested that both men and women suffer more by their partners emotional attachment towards another person.

Similar results in cross-cultural studies are not proof of an evolutional root. It is often difficult to determine what is a result of evolution and what is learned. We also have to note that no gene forces us to behave in a certain way.

The term sex refers to biological aspects of men or women, whereas gender is related to peoples ideas about sexes. Some people feel their sex is not consistent with their gender.

Intersexes are people who have anatomies intermediate between men and women. This can result from gene mutations or atypical hormone levels. The most common cause is congenital adrenal hyperplasia (CHA), in which the adrenal glands are overdeveloped, causing higher testosterone levels than usual.

Hermaphrodites are people wth characteristics of both men and women.

Children with unclear sex are often raised as girls. However, they show more boyish behaviors than girls do (e.g. sexual behaviors).

Testicular feminization (or androgen insensitivity) is a condition in which a person has an XY chromosome pattern but genitals like females.

Cloacal exstrophy is a condition in which a male is born with a smaller penis due to impaired pelvis development. Previously these individuals were raised as girls too, but even after surgeries they often adopt a more masculine identity.

Many individuals who underwent a surgery because of abnormal penis or clitoris in the childhood are dissatisfied later in life. The conclusion: both hormones and the method of raising have significant effects on a child.

Some humans as well other animals show homosexual tendencies. A genetic disposition is greater in men than in women. Men tend to be aware of their homosexuality earlier than women.

Homosexuals differ from heterosexuals in several ways:

1. Heterosexual men have longer arms and legs on average.

2. Homosexual men have bigger right hemispheres.

3. Homosexuals differ in many behaviors not directly linked to sex.

Sexual orientation is not just random decision, but more a complex issue with many affecting factors.

Researchers haven't found any certain gene related to homosexuality yet. Still they have noticed that some genes are more common in homosexuals than heterosexuals. Homosexuality seems to have a genetic basis, at least to some degree.

Homosexual relatives of homosexual men are more common from the mother's side. This fact suggests that a gene related to homosexuality is on the X chromosome.

Genes related to homosexuality cause a problem for the evolutionary perspective: why do those genes survive? Several possibilities have been suggested:

1. Kin selection. Homosexuals might help their sisters and brothers to rear their children.

2. The genes behind homosexuality can be beneficial for females

3. The gene in homozygous form might lead to homosexuality, and the heterozygotic form might lead to benefits in reproduction in heterosexual men.

4. Homosexuality might activate or deactivate certain genes.

Chapter 12 - Emotional behaviors

Defining Emotion

Emotion is a difficult concept to define as we can not easily observe it.

Emotion is usually shattered into three components: cognitions, feelings and actions.

Emotional situations affects the autonomic nervous system (the sympathetic and the parasympathetic). Every situation arouses the autonomic nervous system in a different way.

It is usually assumed that first we feel an emotion and then we give a physiological response to it. James-Lange theory suggests that first comes the physiological response, and the emotion is a response to it. Described be different components, James-Lange theory claims that the order is 1. The cognition, 2. The action and 3. The emotion.

According to James-Lange theory we need to conclude that a person without strong physiological response should feel less emotions, likewise a person with strong response should feel more.

Some people have a condition called pure autonomic failure, in which the autonomic nervous system is impaired. These people should not feel emotions, according to James-Lange theory. However, these people report feelings, but they also report having less intense feelings than before.

The prediction of the response of the autonomic nervous system is situationally dependent.

Researchers have found evidence that smiling increases happiness. However, smiling is not necessary for happiness, for example people with Möbius syndrome (disability to move facial muscles) do experience happiness.

The limbic system is an essential brain area for emotions. Researchers have studied emotions by measuring evoked responses, and using PET and fMRI techniques.

Disgust in the only emotion that might be located in a certain part of the brain (in the insular cortex). All other emotions seem to have cells responding to them all over the brain.

Jeffrey Gray (1970) created a hypothesis about two competing systems:

500. 1. Behavioral activation system (BAS) is linked to left hemisphere activity, causing low or moderate autonomic arousal, with happiness or anger.

     2. Behavioral inhibition system (BIS) is linked to right hemisphere activity, causing arousal, increased attention and inhibits actions. Activates emotions such as fear and disgust.

People with a more active frontal cortex of the left hemisphere are prone to be happier and more outgoing.

The right hemisphere is better at both expressing emotions and decoding other people’s emotions. Localization is so strong that when the right hemisphere is inactive people do not feel strong emotions and do not remember the emotional contents of previous situations.

Emotions have different functions. Fear is a sign that something is threatening us, anger helps us to attack and disgust tells us when to avoid something that might be harmful. Emotions can also be useful at the moment of quick decision.

Emotions are also present when we are making moral decisions. We are able to imagine how other people feel. We tend to decide first, based on our emotions, and then look for a logical justification.

An impairment in the prefrontal cortex causes problems in decision making. People with such damage act impulsively failing to think about consequences.

People with prefrontal cortex damage may never learn moral behavior. Emotions are necessary regarding how we distinguish between good and bad. However, emotions can also interfere with good decisions.

Aggression and Fear

No single reason for all aggressive behaviors can be identified. Both situational and personal factors are present.

An aggressive situation can prime a person to act in an aggressive manner in the future. Priming can be seen in the brain as activity in the corticomedial area of the amygdala.

Environmental factors influence aggression. For example exposure to lead can damage the brain and increase the probability of aggressive behaviors.

A mother smoking during preganancy is known to be connected to aggression. However, mothers who smoke differ from nonsmoking mothers in several other ways. Nicotine damages a developing brain.

Also heredity plays a role. However, the effects of a specific gene on agression were shown to produce only weak effects. Instead, the combination of a genetic predisposition and a difficult early environment seems to be more important.

A low MAOa (monoamine oxidase A) level together with severe maltreatment during childhood predicts antisocial behavior.

Among animals, most aggressive behaviors are due to males fighting for partners and females fighting for their offspring.

In humans, men tend to be more aggressive than women. Testosterone is linked to aggression, though the impact is milder than one might expect.

Testosterone affects several brain areas in different ways, as it increases the activity on emotion-related areas and decreases the conscious ability to recognize emotions.

Aggressive behaviors are linked to low levels of serotonin. In animal studies, social isolation decreased the serotonin turnover (the amount that neurons release and replace, which is estimated from the 5 hydroxyindoleacetic acid (5-HIAA) concentration) in young males. Similar responses might be possible in humans.

Animal studies also indicate that low 5-HIAA levels are related to a shortened life span. From the evolution perspective it is problematic questioning how the responsible genes survive: one possibility is that evolution selects for an average amount of aggression and anxiety. On the other hand, aggression can also be a suitable strategy.

Several researchers have found a link between low serotonin turnover and violent behaviors or suicide attempts.

A diet affects the serotonin synthesis. Tryptophan is an amino acid which is a precursor of serotonin, and other amino acids can block its transport channels.

Tryptophan hydroxylase is an enzyme responsible for converting tryptophan into serotonin. The gene controlling this enzyme differs among people. A less active form is linked to aggressive behaviors.

However, the correlation between serotonin and aggression is not straightforward. Instead, high levels of serotonin can inhibit several behaviors.

Fear

A tendency for anxious feelings, avoidance, or approach depends on the situation. Genetic factors also play a role. The nucleus accumbens is an important brain area.

The amygdala is a key player in the regulation of anxiety.

The startle reflex (the response to loud noise) is used to measure fear or anxiety. The amygdala has cells which respond to rewards, punishments and surprises.

The amygdala regulates the hypothalamus which controls autonomic fear responses. It is also connected to the prefrontal cortex, which controls avoidance and approach responses.

An impaired amygdala causes problems concerning the learning of fear responses. However, previously learned fear responses function better.

The Klüver-Bucy syndrome is a condition which can result following damage in the amygdala. It is characterized by tameness and calmness.

Attention to any kind of emotional stimulus raises the amygdala’s responses to the relevant stimulus.

The direction of other people’s expressed emotion is also meaningful. We tend to respond quicker to angry expression when it is directed towards us and to fearful expression when it is directed somewhere else.

The amygdala also responds to stimuli which are not recognized consciously.

Urbach-Wiethe disease is a rare condition in which the amygdala can be impaired by accumulated calcium. The patients have problems detecting weak emotional signals.

People with an impaired amygdala fail to focus on emotional stimuli in a normal manner. The reason why damage to the amygdala impairs recognition of fear is that these people tend to focus on the nose and mouth, not the eyes.

Drugs used to reduce anxiety alter activity at amygdala synapses. GABA inhibits anxiety responses. Cholecystokinin (CKK) is a neuromodulator which increases anxiety.

Benzodiazepines are the most commonly used drugs against anxiety (e.g. diazepam, alprazolam). They bind to GABAa receptors. Side effects of bezodiazepines are for example sleepiness and memory problems.

Endozepines (such as diazepam-binding inhibitor) block the effects of benzodiazepines.

Stress

Behavioral medicine stresses people's own decisions (e.g. smoking, exercise etc.)

Hans Selye (1979) suggested the general adaptation syndrome, which is a response to stress.

The syndrome has the following phases:

• The alarm stage: activation of the sympathetic nervous system

• The resistance stage: sympathetic response decreases, cortisol and other hormones are secreted thus maintaining alertness, resisting infections and healing wounds.

• The exhaustion stage: is a result of prolonged stress. A person is tired, inactive and vulnerable because the body is not able to maintain those heightened responses.

Many kinds of events can cause stress, even positive events. Stress-related diseases are common in Western societies, in which we confront several stressful events.

Two body systems respond to stress:

• The sympathetic nervous system: fight or flight.

• The HPA axis, which includes the hypothalamus, pituitary gland and adrenal cortex. The hypothalamus stimulates the pituitary gland to secrete adrenocorticotropic hormone (ACTH), which activates the adrenal cortex to secrete cortisol.

Cortisol increases metabolic activity and is usually considered to be a “stress hormone”. Cortisol improves attention and memory, but prolonged secretion of cortisol can impair the memory and immune systems.

The immune system fights against viruses, bacteria and other threats.

An autoimmune disease is a condition in which the immune system is too efficient and attacks the body’s own cells.

There are several types of leukocytes (white blood cells):

• B cells, which secrete antibodies (proteins that attach to certain antigens). Antigens are proteins on the cell’s surface. The B cells recognize a body’s own antigens and attacks foreign ones.

• T cells attack intruders directly. Some T cells also help other B cells and T cells to multiply.

• Natural killer cells attack all intruders. They can fight against tumor cells and cells that are infected with viruses.

Cytokines are proteins that also fight against intruders and communicate to the brain that the body is sick. Cytokines incite the hypothalamus to create fever, lack of appetite and energy, and sleepiness.

The immune system also produces prostaglandins, chemicals that increase sleepiness.

Psychoneuroimmunology is a study which focuses on the relationship between the nervous system and immune system.

Stress has many effects on the immune system. It increases its production of natural killer cells and cytokines. Cytokines help to resist intruders, but they also give the same response as though the body were ill.

Prolonged stress reactions are harmful for the body. It is suggested that when the energy is used on increased metabolism, there is not enough energy for synthesizing proteins (as the ones of the immune system).

Long lasting stress increases the probability of illness. Prolonged stress can also impair the hippocampus.

There are several ways to decrease stress. One of most efficient is social support. Also exercise, breathing routines and meditation can work.

Posttraumatic stress disorder (PTSD) is a condition which occurs after highly stressful life-events. The symptoms, which last at least a month after the event, include nightmares, flashbacks, and exaggerated arousal as a response to stimuli.

Some people are more vulnerable to PTSD than others. A smaller than average hippocampus and lower than average cortisol levels seem to be linked to PTSD.

Chapter 13 - The biology of learning and memory

Learning, Memory, and Amnesia

Ivan Pavlov was first to present classical conditioning. Classical conditioning involves presentations of a neutral stimulus along with a stimulus of some significance, the 'unconditioned stimulus'. Presentation of the significant stimulus evokes an innate response. Pavlov called these the unconditioned stimulus (US) and unconditioned response (UR), respectively. If the neutral stimulus was presented along with the unconditioned stimulus, it would become a conditioned stimulus (CS). If the CS and the US are repeatedly paired, eventually the two stimuli become associated and the organism begins to produce a behavioral response to the CS. Pavlov called this the conditioned response (CR).

Operant conditioning works through reinforcers and punishments. A reinforcer increases the probability of a response in the future, a punishment decreases it.

However, animals have several methods of learning and usually they are difficult to label. The method of learning is also situationally dependent.

Pavlov suggested that learning is based on the growth of connection between two brain areas. Karl S. Lashley proved it does not depend on the connections across the cortex. Lashley looked for the engram; the physical representation of what has been learned.

Richard F. Thompson presented that lateral interpositus nucleus (LIP), a part of the cerebellum which is important for learning.

The memory system can be divided into two categories:

• Short-term memory is the part of the memory which new information enters first.

• Long-term memory is a larger storage of memories. If a new information is consolidated in the short-term memory it will enter long-term memory.

However, the distinction between these two is not clear. Also the term working memory is presented as an alternative for short-term memory.

Delayed response task is a commonly used procedure to test working memory.

Elderly people tend to have problems with working memory, maybe because of changes in the prefrontal cortex.

Amnesia refers to the loss of memory. Anterograde amnesia is an inability to remember events that happened after the brain damage. Retrograde amnesia is an inability to remember events that happened before the brain damage.

Most people with amnesia have normal short-term and working memories.

Episodic memories are memories of single events.

Imagining future events is to memorize past similar events and to modify them. People who have amnesia therefore cannot imagine future events.

Explicit memory consists of the deliberate recall of information. On the contrary, implicit memory refers to the influence of previous experience on behavior, which a person is not necessarily aware of. Most people with amnesia have better implicit than explicit memory.

Declarative memory is the ability to memorize in words, procedural memory refers to motor skills and habits. People with damage to the hippocampus usually have impaired declarative memory but good procedural memory.

The hippocampus seems to be the more important area for declarative memory, as the basal ganglia is more important for procedural memory. Nevertheless, most tasks combine different kinds of memory systems.

The hippocampus seems to also be important for spatial memory, and it can even grow after extensive learning experiences.

It is suggested that the hippocampus is also related to remembering the details and the context of an event. Thinking of recent memories activates the hippocampus, when it comes to older memories the answer is less straightforward.

Memories with strong emotional content are more easily consolidated – this is due to secretion of cortisol.

Korsakoff’s syndrome is a brain damage characterized by memory loss, confusion and melancholy. It is caused by prolonged thiamine (B1 vitamine) defiency. People with Korsakoff’s syndrome have problems in reasoning their memories. They also tend to confabulate (fill their memory gaps by guessing).

Alzheimer’s disease is another reason for memory loss. People with Alzheimer’s disease have better procedural than declarative memory. Genes play an especially important part in the early-onset Alzheimer’s disease.

Other than the main areas related to memory processing, almost the entire cortex and several subcortical areas are important for memory.

Semantic dementia refers to the loss of semantic memory, and it is caused by impaired anterior and inferior regions of the temporal lobe.

Storing information in the nervous system

Patterns of electrical activities leave paths on the brain. Pavlov’s studies on classical conditioning were the first ones regarding the physiology of learning. Once the connection between two neurons is made, it is easier to create next time.

The Hebbian synapse refers to a synapse that increases in effectiveness as a result of activity in the presynaptic and postsynaptic neurons.

Adaptation means decreased response to a stimulus when the stimulus is repeated several times. It is not due to muscle fatigue or decreased response of the sensory neuron.

Sensitization means increased response to weak stimulus after exposure to more intense stimulus. Molecular events behind sensitization are serotonin blocking potassium channels of a presynaptic neuron, and continuing the release of transmitter from that neuron.

Changes in a synapse can change behavior.

Long-term potentiation (LTP) refers to the strengthening of response in some synapses because of an intense series of stimuli conducted toward a neuron. Some properties make LTP a plausible possibility for the molecular basis of learning and memory: specificity, cooperativity and associativity.

Long-term depression (LTD) is the opposite process to LTP. It occurs at the same time: as one synapse strengthens, another weakens.

Usually LTP depends on changes at glutamate synapses. Two types of glutamate receptors (AMPA and NMDA) are presented.

When glutamate excessively stimulates AMPA receptors, the NMDA are stimulated too. That leads calcium to flow into the cell, which alters a cells future responsiveness to glutamate at AMPA receptors.

Once LTP happens, the AMPA receptors stay tuned. Often LTP is linked to increased release of neurotransmitter from the presynaptic neuron.

LTP does not take place during ‘’traditional” learning, also when exploring new environment, receiving repeated stimulation and creating drug addiction.

Some drugs can enhance learning, such as caffeine as it increases arousal. Ginkgo biloba is a herb which might have similar effects on some people. Other possible drugs work on glutamate or dopamine synapses.

Chapter 14 - Cognitive functions

Lateralization of Function

Many things in nature are symmetrical. The few exceptions are interesting, for example different functions of hemispheres.

Most information is processed in the contralateral hemisphere. However, taste and smell are uncrossed and both hemispheres have control over the trunk and facial muscles.

The corpus callosum is the place where two hemispheres exchange information. Other areas with similar functions are the anterior commissure, the hippocampal commissure and few other commissures.

Lateralization refers to the fact that the hemispheres operate on different tasks.

The left visual field (field that is visible all the time) projects onto the right half of the retina, which sends information to the right hemisphere. The opposite pattern is seen on the right visual field.

The auditory system is a bit different, as each ear sends information to both sides of the brain.

Epilepsy is a condition which manifests itself through excessive synchronized neural activity. The possible causes of epilepsy are brain tumors, toxic substances, gene mutations, brain infections or trauma. In epilepsy the release of the inhibitory neurotransmitter GABA is decreased. Drugs which combat epilepsy enhance GABA.

Severe epilepsy can be treated with surgery, in which the focus is removed. If a person has many foci, surgeons can cut the corpus callosum, the result is epileptic seizures will occur only on the other half of the body and they are less frequent.

The term split-brain people refers to individuals with a cut in the corpus callosum. They can easily use both hands independently, but using them together in unfamiliar tasks causes trouble. The left hemisphere is dominant for speech production for most of the people. When it comes to non-language sounds the hemispheres are equal.

A person in split-brain condition can name objects seen in the right visual field, but not objects seen in the left visual field. Many people with bilateral control of speech tend to stutter – in this sense control of speech happening only on the other side can be beneficial.

When the corpus callosum is cut once, it does not heal. However, the two hemispheres learn how to cooperate using the other connections. The left hemisphere tends to be dominant sometimes and therefore take the control.

The right hemisphere is better at detecting other people’s emotions. Therefore a person with damage in the left hemisphere performs somewhat better in tasks requiring understanding other people’s feelings, as that hemisphere is not disturbing the right one.

An impairment in the right temporal cortex can result in disability to remember the visual features of objects. One hypothesis suggests that the left hemisphere is better at detecting details, as the right hemisphere detects overall patterns.

The differences between the two hemispheres can be seen also in healthy people.

Humans have innate ability to differentiate between sounds. The hemispheres differ slightly from each other from the very beginning, for example the planum temporale (a part of the temporal cortex) is usually larger in the left hemisphere. Also the left hemisphere is specialized in language already. The corpus callosum develops fully between ages 5 and 10. For this reason young children may act in a way which is similar to split-brain people. In the beginning the corpus callosum has more axons than it will have by the end of the maturation process. The reason for this is that two neurons connected by the corpus callosum need to have corresponding functions. Development refers to the selection of certain axons while others are discarded.

Some people are born without the corpus callosum. However, those people differ from split-brain people, as they are able to do many things split-brain people are not. For example, they can verbally describe what they see on either visual field – this is possible because they do not use the right hemisphere for speech. Furthermore, the brain’s other commissures become larger.

For almost all right-handed people the left hemisphere is responsible for speech. Left-handed people show more variation.

Most tasks require the cooperation of both hemispheres.

Evolution and Physiology of Language

Most animals have several ways to communicate: visual, auditory, chemical etc. Human language is unique because of its productivity (ability to produce new signals to present new ideas). It is reasonable to assume that other species also show some rudimentary basis for language. Actually the assumption is right: for example chimpanzees can learn some visual language systems.

Bonobos, one chimpanzee species, resemble humans in many ways. Studies have shown their superior ability to learn language, which might be a result of differences between species, training during sensitive periods, or different training methods.

Also African gray parrots show impressive learning abilities when it comes to language.

Studies among non-human animals can give insight into how to teach a language to someone with learning problems (e.g. autistic children, brain damage patients). They also show an evolutionary basis of language.

Two hypotheses have been presented to explain why people have a better ability to learn language compared to other species:

• Language was a by-product of overall brain development. This theory has some severe problems. The first being that genes can impair language abilities without impairing intelligence. Another point is a condition called Williams syndrome – a person is mentally retarded but his/her language is fairly fluent.

• Language evolved as a specialized brain mechanism. Noam Chomsky and Steven Pinker claimed that we have innate mechanism for learning language, called language acquisition device. They suggested that children learn a language so easily that such a mechanism must exist. Furthermore, Chomsky suggests that children are born with grammatical rules; this is called the poverty of the stimulus argument. Most researchers agree that humans have evolved something that makes them learn language with ease, but the debate about that something continues.

Language learning probably has an early sensitive period, even though there is no sharp cutoff age.

When learning a new language, children become familiar with pronunciation and grammar quicker, but adults learn the vocabulary easier.

Aphasia refers to language impairment. It is often a result of damage in the Broca’s area, when it is called Broca’s aphasia or non-fluent aphasia.

People with Broca’s aphasia also have trouble in other ways of expressing themselves (writing, gesturing), not just speaking. When they speak they tend to avoid closed class of grammatical form (prepositions, conjunctions etc.) and use only open class terms (nouns and verbs). The problem is with word meanings and not just pronunciation. They do have some knowledge of grammar, even though they do not know how to use it.

Another form of aphasia is Wernicke’s aphasia (also fluent aphasia), which is a result of damage in the left temporal cortex. A person with Wernicke’s aphasia can speak and write fluently but their language comprehension is weak and they have problems remembering the names of objects (anomia).

Bilingual speakers use the same brain areas for both languages. However, when they use the weaker language, it activates those brain areas more.

Both language and music exist in every human culture. They have many parallels, which suggest that they evolved together.

Dyslexia is a reading impairment, when a person has otherwise proper academic skills and vision. Dyslexic people have some minor brain abnormalities, for example bilaterally symmetrical cerebral cortex.

Reading problems differ from each other. One distinction is made between dysphonetic dyslexics (problems in sounding out words) and dyseidetic dyslexics (failure to recognize the word as a whole).

Many people with dyslexia have auditory problems and trouble detecting the temporal order of sounds, as well as problems with attention.

It might be helpful for a dyslexic person to focus on just one word at a time.

Consciousness and Attention

Consciousness is a difficult concept to define. The operant definition is: If a cooperative person reports the presence of one stimulus and cannot report the presence of a second stimulus, then they are conscious of the first and not of the second.

The definition above cannot be applied for example to animals or infants. Attention is a closely related concept.

Inattentional blindness (change blindness) refers to the fact that we are conscious of only the things to which we direct our attention.

The consciousness of a stimulus is linked to the amount and spread of brain activity. A conscious stimulus also induces precise synchrony of responses in several areas of the brain.

Binocular rivalry occurs when two different stimuli compete for attention.

According to research, consciousness is an all-or-nothing phenomenon: that is, it has a threshold.

A meaningful stimulus captures attention faster than a meaningless stimulus; ergo the brain somehow processes the stimulus before coming conscious of it.

Also later events give meanings to some events, so that we become conscious afterwards.

Spatial neglect is a condition in which a person ignores the left side of the body or the left side of objects. It is caused by damage to the right hemisphere.

In spatial neglect the problem is not impaired sensation, but attention. Only telling a person to focus on the neglected side can increase attention.

Usually people with neglect also have problems in spatial working memory and with shifting attention.

Chapter 15 - Mood disorders and schizophrenia

Mood Disorders

In mental disorders both mental basis and experiences are important factors.

Several issues can be triggers for depression: traumatic experiences, genes, hormones, tumors, head injuries etc.

Major depression differs from normal sadness in that it is a prolonged condition. The symptoms are suicidal thoughts, concentration problems, lack of energy and pleasure, sleeping problems and feelings of helplessness. It is more a lack of happy feelings than just sadness.

Depression is quite a common disorder, as 10% of people have it during the lifespan. It is more common in women than men.

Most depressed people can name the event that triggered the condition. However, depression usually occurs in episodes and later episodes do not necessarily need a trigger.

Heritability of depression is moderate. Depression is more probable among people who have a female relative with early-onset depression.

Several depression related genes have been found. One such gene controls the serotonin transporter protein, and it has the long type and the short type. These two types occurring together increase the risk of depression. However, these genes are more related to the sensitivity to environmental influences than depression itself.

Some cases of depression are related to viral infections, for example Borna disease seems to cause depression.

Postpartum depression is a form of depression that is launched after giving birth. Usually it goes away with time. The probability of postpartum depression is higher among women who have suffered depression before.

A happy mood is linked to activity on the left prefrontal cortex. Usually people with depression have an active right prefrontal cortex and a less active left prefrontal cortex.

We can divide antidepressant drugs into four categories:

• The tricyclics, which block the transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron. The result is that neurotransmitters continue stimulating the postsynaptic cell. As a side effect the tricyclics also block histamine and acetylcholine receptors causing drowsiness and urinating difficulties among other things.

• The selective serotonin reuptake inhibitors (SSRIs), which are like tricyclics but specific to serotonin. Therefore their side effects are milder.

• The monoamine oxidase inhibitors (MAOIs) which block monoamine oxidase (MAO). MAO is an enzyme in the presynaptic terminal that metabolizes catecholamines and serotonin into an inactive form. MAOIs are often prescribed after ineffective use of SSRIs and tricyclics.

• The atypical antidepressants which are antidepressants that do not fit previous categories, for example an herb called St. John’s wort, which operates like SSRIs.

Most people with depression recover even without treatment. About 30% recover in a few weeks without treatment or with placebo, about 20% respond to either antidepressants or psychotherapy, and a bit over 20% to both of them.

Antidepressants are not very efficient for people with mild depression. Also patients with early childhood trauma (e.g. abuse) respond better to psychotherapy.

There is a debate going on whether antidepressants should be prescribed to children and adolescents or not. Some studies suggest that antidepressants can increase the suicidal risk in children and adolescents.

The way antidepressant drugs work is still partly unclear. Depression is not just a result of neurotransmitter deficit. Antidepressants affect synaptic activity soon after taking them but their behavioral effects come later (after 2 weeks).

Electroconvulsive therapy (ECT) is treatment using an electrically induced seizure. Nowadays it is used on patients who do not respond to antidepressants. The most common side effects are memory loss and another depressive relapse. However, ECT is a rather effective and quick method.

Both ECT and antidepressants operates by increasing the proliferation of new neurons in the hippocampus. Another method similar to ECT is repetitive transcranial magnetic stimulation. It is a moderately effective treatment for depression.

Depression affects the sleeping behaviors of a person. Depressed people tend to awaken early and have problems falling asleep again. People who are predisposed to depression have a lifelong trait of altered sleep.

The quickest known method for curing depression is one completely sleepless night. It also increases the proliferation of neurons in the hippocampus.

Regular exercise is also a good treatment for depression, especially when combined with other treatments.

Depression can be divided into two categories:

• Unipolar depression, in which a person’s mood varies between normality and depression.

• Bipolar depression, in which a person has mood swings between depression and mania.

A person in mania has excessive self-confidence, feelings of excitement and has problems with inhibiting his/her behavior. Bipolar disorder also has a hereditary basis, and two genes have been found to increase the risk. However, we have to note that they do not determine anyone’s bipolar disorder. Antidepressants are not a suitable treatment for people with bipolar disorder. Instead, lithium salts have proved to be effective. Also drugs called valproate and carbamazepine are used.

Excessive glutamate activity can result in mania. All the drugs mentioned above decrease the number of AMPA type glutamate receptors in the hippocampus.

The sleeping patterns of people with bipolar disorder are also altered, as they tend to suffer from sleep deprivation during mania and sleep too much during depression. One possible treatment is to maintain a similar sleeping schedule during different phases.

Seasonal affective disorder (SAD) occurs during a certain season, for example winter time. It is most common near the poles. Usually it is not as severe as major depression. Contrary to other patients with depression, people with SAD have phase-delayed sleep and temperature rhythms.

Schizophrenia

Schizophrenia is characterized by hallucinations, delusions, impairments in thinking and moving, and inappropriate emotional expressions. The symptoms vary between individuals to a great extent.

Schizophrenia can manifest itself either as acute or chronic. Acute schizophrenia has a sudden onset and the probability of recovery is high. In chronic schizophrenia the onset is gradual and the possible recovery takes longer.

The term schizophrenia refers to “split mind”, which denotes the differentiation between the emotional and intellectual side of experience.

The symptoms of schizophrenia fit two categories:

• Positive symptoms are symptoms that occur even though they should be absent. Positive symptoms are either psychotic (e.g. delusions and hallucinations) or disorganized (e.g. extraordinary behaviors, incoherent speech etc.).

• Negative symptoms are symptoms that do not occur even though they should, for example impairments in working memory and social interactions.

One of the central symptoms of schizophrenia is disordered thinking, as well as memory impairment. About 1% of people develop schizophrenia during the lifespan. It is most common in the US and Europe, and a bit more common in men than women.

Schizophrenia is related to high dopamine levels in the brain, and men’s brain release more dopamine than women’s, which could be an explanation for the previous fact. Schizophrenia has a genetic basis, at least to some degree, but no certain gene causes it. The closer a relative is with schizophrenia, the greater the risk to develop it. Monozygotic twins show about 50% concordance (agreement).

Studies exploring the genes related to schizophrenia are controversial. One of the genes that seems to be more common among schizophrenics is DISC1 (disrupted in schizophrenia 1).

It is reasonable to assume that any specific gene for schizophrenia would have disappeared during evolution. One hypothesis is that many cases of schizophrenia arise from new mutations. The fact that children with schizophrenia more frequently have older fathers supports this hypothesis.

The neurodevelopmental hypothesis suggests that schizophrenia is related to extraordinary prenatal (before birth) or neonatal (newborn) development of the nervous system. Researchers have found that poor nutrition of the mother, complications at the time of delivery, head injuries and low birth weight have connections to schizophrenia.

Mother’s and child’s inconsistent Rh-factors increase the probability of schizophrenia.

The season-of-birth effect refers to the fact that babies born during wintertime have a slightly higher probability of developing schizophrenia. The cause might be complications of delivery or early nutrition, or viral infections (which are more common in the fall).

Some infections during childhood can also increase the risk of schizophrenia, for example Toxoplasma gondii, a parasite carried by a cat.

Schizophrenia is characterized by some mild brain abnormalities, which are small and vary a lot:

• Deficits on the left temporal and frontal areas of the cortex, as well as on most of the cortical areas.

• The thalamus is smaller.

• The ventricles are larger; the brain cells have less space.

• Some areas are slower to mature, for example the dorsolateral prefrontal cortex (impairments in memory and attention).

• Cell bodies are smaller, especially in the hippocampus and prefrontal cortex.

• Less activity in the left hemisphere.

These changes can be reasons for schizophrenia or as a result of treatment. It is unclear whether brain alterations are progressive (do they increase over time).

Usually schizophrenia is diagnosed after the age of 20. However, most of those people show signs already in childhood, for example memory and attention problems. The late onset can be explained by slowly maturing brain areas.

Drugs used to treat schizophrenia are antipsychotic (or neuroleptic) drugs. They are divided into two groups:

• The phenothiazines, which include chlorpromazine.

• The butyrophenones, which include haloperidol.

The dopamine hypothesis of schizophrenia claims that the basis of the disorder is a result of the excessive activity at dopamine synapses in specific brain areas. Substance-induced psychotic disorder supports this theory. However, there are some problems with this theory. Antipsychotic drugs block synapses in just a few minutes, but the behavioral alterations take several weeks.

The glutamate hypothesis of schizophrenia claims that the reason is linked to inactive glutamate synapses especially in the prefrontal cortex. Dopamine and glutamate have a connection so that dopamine inhibit glutamate release or glutamate can stimulate neurons inhibiting dopamine release, which would explain abnormal dopamine levels too.

A drug called phencyclidine (PCP) inhibits the NMDA glutamate receptors and is known to produce schizophrenic symptoms in larger doses. Glycine increases the effectiveness of glutamate, and therefore glycine can increase the activity in NMDA.

Drugs used to treat schizophrenia block dopamine synapses in the mesolimbocortical system. As a side effect they also affect mesostriatal system, causing tardive dyskinesia (condition with tremors and involuntary movements).

Second-generation antipsychotic drugs (e.g. amisulpride, risperidone) do not cause these problems, but they have other severe side effects, for example impairment of the immune system.