Executive functions modulate the activity of other cognitive functions in a flexible and goal-directed manner. They perform a supervisory or regulatory role. Flexible: depending on the current contextGoal-directed: to achieve the current goalTaxonomy of executive functions: Intelligence:Charles Spearman: central intelligence factor ‘g’Cattell: division betweenFluid intelligence: ability to solve abstract reasoning problemsCrystallized intelligence: learned procedures and knowledgeFluid intelligence correlates highly with measures of executive functionsExecutive functions in the brain are mostly regulated in the prefrontal cortex. The anterior cingulate cortex and the parietal cortex are also important. The caudate nucleus and putamen (basal ganglia) are also important for executive functions. Frontal-cortex-basal ganglia loops: Damage to the PFC: cognitive function appears to be normal and unimpaired. But there is impairment in forming, updating and implementing rules for appropriate or effective behavior. This can lead to profound difficulties carrying out simple activities. Damage can lead to:Dysexecutive syndrome: lack of initiation, socially quiet. Disinhibition syndrome: lack of inhibition, socially too expressiveEnvironmental dependency syndrome: actions not based on goals but on surrounding environment. Used imitation and utilization. Miller & Cohen model: cognitive control stems from the active maintenance of patterns of activity in the prefrontal cortex that represent goals and the means to achieve them. Switching between rulesWisconsin Card Sorting TestThe orbitofrontal cortex: shifting between rules for behaviorReversal learning: rules mapping of stimuli to rewards switch unexpectedlyDamage to OFC: trouble switching between rules.Relating rules: reasoning. Deduction: truth of a conclusion must be deduced solely from a set of premises that is already at handInduction:...


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      Cognitive Neuroscience - Lectures (Utrecht University)

      Lecture 1 - Introduction & EEG (Cognitive Neuroscience, UU)

      Lecture 1 - Introduction & EEG (Cognitive Neuroscience, UU)

      Franz Joseph Gall suggested that surface of the head depends on mental skills. He is one of the firsts linking the brain to cognition.

      Can modern phrenology be seen as modern cognitive neuroscience?

      • Yes:
        • Functional differentiation of the brain
      • No:
        • Functions are defined by thorough experimentation
        • Multidisciplinary research
        • Not just size of brain areas

      Brodmann was the first to map the cortex based on cell types. More detailed maps followed later.

      The structure of the brain has a reason: function.

       

       

       

      You can measure brain activity using

      • Action potentials (electrophysiology)
      • local field potentials (electrophysiology)
      • Electromagnetic field at scalp (EEG/MEG)
      • Manipulating neural activity (TMS/tDCS)
      • Blood oxygenation (fmri)

      Brain elements: neurotransmitter & hormones. You can add pharmacology and food supplements.

      Brain computation: making models of the brain to improve applications (facebook, google).

      Cognitive neuroscience defines steps/networks in information processes by using neuroscientific methods.

      EEG (ElectroEncephaloGraphy):

      • Measures the differences in voltage across the scalp
      • Reflects post-synaptic potentials (PSP): difference in voltage along axons.
      • Both inhibitory and excitatory psp
      • Reflects local field potential  not a single action potential but a summation of many neurons

      When is the measurement good?:

      • Mass activity
      • Synchronized activity
      • Close to the scalp

      32-64 electrodes are enough to measure time effects.

      Advantages EEG:

      • Temporal characteristics
      • ERP’s

      EEG measures the voltage potentials and MEG measures the magnetic field. MEG is similar to EEG, but better localization and most sensitive to activity originating from sulci.

      EEG = relatively cheap, measures more neurons.

      MEG = expensive, better localization

      EEG & MEG same temporal resolution, MEG better spatial resolution.

       

       

       

       

       

       

       

      So slow waves = low arousal

      Fast waves = high arousal

      Gamma (32Hz>) = superlearning

      Beta (16-31Hz) = processing information, analytical thinking

      Alpha (8-15Hz) = Eyes closed or very relaxed

      Theta (4-7Hz) = Sleep, REM, dreaming, deep meditation

      Delta (<4Hz) = deep dreamless sleep

       

      ADHD = hyperactive, but less cortical arousal

      Treating ADHD = increase arousal with medicine

       

      Each frequency reflects a different mental state.

       

      Average ERP’s to cancel out the noise.

       

       

      Questions? Let me know in the contribution section!

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      Lecture 2 - fMRI & Visual Perception (Cognitive Neuroscience, UU)

      Lecture 2 - fMRI & Visual Perception (Cognitive Neuroscience, UU)

      Diffusion-weighted imaging – measures the direction of water movement by comparing responses to magnetic fields in different directions. Shows neural fibre bundles.

      Functional MRI – measures how tissue magnetic interactions change over time. Examines the blood flow and oxygenation. Neural activity changes when subject is exposed to a stimulus.

      MRI & fMRI advantages:

      • High spatial resolution
      • Straightforward analysis / interpretation
      • Safe and non-invasive
      • Easy access

      Disadvantages:

      • Indirect measure of neural activity
      • Low signal to noise rations
      • Awkward environment
      • Poor temporal resolution

      How does MRI work?

      1. Place brain in a strong static magnetic field
      2. Use weaker, changing magnetic field to change magnetization energy
      3. Remove gradient field
      4. Measure energy emitted and reconstruct into image
      5. fMRI: measure changes/distortions produced by magnetically-active substances

      The signal depends on:

      • PD: proton density
      • T1: realignment with magnetic field
      • T2: proton misalignment due to tissue interactions
      • T2*: T2 and magnetic field inhomogeneities

      Deoxygenated blood causes signal loss.

      Why does fmri work?:

      1. Deoxyhemoblobin affects T2*
      2. Blood response follows neural activity
      3. Step 2 overcompensates

      Important: effect 2 does not compensate accurately for effect 1

      So oxyhemoglobin concentration increases due to increased blood flow.

       

      Relation between neural activity and BOLD (black is neural activity):

      [note: deze afbeelding uit het college is door de WorldSupporter redactie verwijderd wegens vermoedelijke inbreuk op het auteursrecht] 

      • MUA: action potentials (spikes) = neural output

      LFP: synaptic activity = neural processing

      fMRI is slightly better correlated with LFP. So BOLD signals reflect synaptic activity.

       

      What limits the temporal resolution of fMRI?

      • Slow blood flow changes
      • NOT frequency of measurement

      Perception: a translation of the physical environment into a pattern of neural activity that can be used by our brain to guide behavior. Perception is a set of tricks to extract useful (not an accurate!!) information from the environment.

      The ganglion cells look at change in color: contrast.

      Visual convergence:

       

       

      We need to match the details of the image to the properties of the (visual) cell:

       

       

      So the top cell responds well to the first image and the bottom cell responds well to the third image. So we use the differently sized receptive field cells to perceive different properties in images.

      The images we see is mapped in the visual cortex:

       

      Orientation-cells only respond to cells in a specific orientation. This is the relation between preferred orientation and track distance:

       

      There are two visual pathways:

      • Dorsal visual stream: where
      • Ventral visual stream: what

      V2 looks for patterns in the images it receives. V1 does not.

      The middle stages of visual processing look at common

      .....read more
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      Lecture 3 - Single Unit Recording & Audition (Cognitive Neuroscience, UU)
      Lecture 4 - Motor system (Cognitive Neuroscience, UU)

      Lecture 4 - Motor system (Cognitive Neuroscience, UU)

      There are two types of movement:

      • Automatic movements (reflexes)
      • Volitional movements (self-controlled)

      The motor system has a hierarchical organization:

      • Peripheral
        • Nerves from spinal cord to muscles
        • Somatic (voluntary) and autonomic (involuntary)
      • Central
        • Spinal cord
        • Brainstem
        • Subcortical (basal ganglia)
        • Cortex (primary motor cortex, premotor cortex, PCC and SMA
        • Cerebellum

      Motor sensor loop:

      • Sense
      • Move
      • Sense & feedback
      • Move
      • Sense & feedback
      • Adjust or strengthen internal motor plan
      • New movement etc,

      For rapid targeted movement, there is a primary fast ballistic movement, and then an error-correction movement.

      Activating muscles through acetylcholine release. Then the muscle contracts.

      Motor neurons are controlled by the central nervous system through the spinal cord. They are relatively large and are arranged in antagonistic (opposite) pairs.

      Reflex arc: simple and short circuit for fast response. A reflex happens in the spinal cord and spinal neurons can generate an entire sequence of movements without feedback or input.

      What happens when the sensory nerves are destroyed, but motor nerves are spared? No error-correction --> errors accumulate during sequences of automatic actions.

      Summary peripheral motor system:

      • Mechanism on its own in non-primates
      • Strong dependence on central nervous system in humans

      Central nervous system: there are different tracts responsible for different motoric functions:

       

       

       

       

       

      Primary motor cortex:

      • Simple movements, mapping body parts (overlap)
      • Large Betz cells  direct connections to alpha motor neurons in spinal cord. Only get activated in response to a very specific type of movement
      • Damage: Relatively common. Paralysis to contralateral lesion sire. Reflexes become stronger.
      • Is interconnected to surrounding regions, such as pre-motor cortex

      Pre-motor cortex:

      • Closely linked to primary motor cortex. Sends signal to primary motor cortex to achieve moment
      • Also closely linked to higher-order areas (frontal). Sends signal to adapt movement depending on context.
      • Closely linked to thalamus.
      • Activity reflects planning and goal depending on context
      • Damage: no response to cues, anosognosia (unaware of inability).

      Posterior Parietal Cortex

      • Important for sensory feedback and control of movements
      • Controls externally-generated movement: perception action coupling
      • Attention & gaze are coded in the parietal cortex
      • Damage: difficulty with vision-based motor adjustment (apraxia)
        • Ideomotor apraxia: (imitation of) action after instruction is disrupted. Unable to create an action concept
        • Ideational apraxia: know what the desired sequence of actions is, but can’t execute it correctly

      Supplementary Motor Area (SMA)

      • Planning internally-generated sequence movements (specifically learned movements, such as playing the piano).
      • Damage: defects in motor sequence planning.
      .....read more
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      Lecture 5 - Stimulus processing (Cognitive Neuroscience, UU)

      Lecture 5 - Stimulus processing (Cognitive Neuroscience, UU)

       

      Attention is selective. Selective attention refers to the allocation of processing resources, generally at the expense of resources allocated to other stimuli.

      Neuroscientific concept: attention is the manipulation of activity of population of cells that process sensory information.

      Advantages of attention:

      • Detailed representation of stimuli
      • Faster and more accurate response to stimuli
      • Better memory of stimuli, better decision-making, etc.

      Disadvantage: opposite effect for unattended stimuli.

       

      Arousal is not attention. Arousal modulates all sensory signals  baseline effect

      Attention selects and modulates specific sensory signals  selection effect

      Two forms of attention:

      • Overt attention: you look at what you want to attend
      • Covert attention: you attend something that is outside your gaze

      Internal manipulation of attention: you decide yourself what you attend. This is endogenous, top-down or controlled attention.

      External manipulation of attention: sensory stimulus characteristics decide what you attend. This exogenous, bottom-up, reflexive attention. The sensory area is shaped by experience over years. It responses to most relevant things due to experience.

      --> Salience models: models that predict what you attend automatically.

       

      Attentional blindness

      • You cannot process everything at the same time: loss of information.
      • Can be measured using the change blindness paradigm

      Attentional blink

      • Try to detect the white target
      • As you are busy with target 1, target 2 is missed

      Attentional cueing

      • Posner’s cueing task
      • Recognition of target is better and faster for congruent cue, and worse for the incongruent cue
      • Same applies to exogenous cue

      Cocktail party

      • People prefer one auditory stream of information over another
      • Ignoring one stream is called shadowing

      Visual search

      • Quickly finding an item in a clustered environment

      Neural mechanisms are strengthened when attention is given to it.

      Question 1 can be answered using EEG: great temporal resolution.

      • Also auditory attention: compare ERP to attended vs. unattended stimuli
      • BER is unaffected by attention
      • P20-50 and N1 are evoked by attention

       

       

       

       

      Attention is necessary for similarity analysis.

      Mismatch negativity (MMN): oddball paradigm.

      Feature attention: the amplitude is increased for attended stimuli and the sensitivity is narrowed.

      --> Attention acts in the brain area that codes the target feature.

      • Orientation: V1
      • Color in V4
      • Motion in MT+
      • Faces in FFA
      • Pitch/frequency in auditory cortex

       

      Spatial attention: attention to location in a visual field. Could be an auditory source.

      Receptive field: area of interest to the neuron. A neuron responds when a stimulus is shown in its receptive field.

      Each cell has a receptive field: responses only to a specific

      .....read more
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      Lecture 6 - Control of attention (Cognitive Neuroscience, UU)

      Lecture 6 - Control of attention (Cognitive Neuroscience, UU)

      Shifts of attention are useful for many daily tasks, such as finding your keys, playing video games, learning, personality and flexibility and efficiency.

      Patients with attentional deficits have damage to the frontoparietal network, causes:

      • Visual Neglect
      • Balint’s syndrome

      Neglect

      • Hemispatial unilateral neglect: left side of the visual field is neglected, due to right inferior lobe damage. Right side neglect is less common due to processing of right space by both hemispheres
      • Ideational apraxia: misuse of tools, due to left inferior parietal lobe damage
      • Can become covertly aware of stimulus
      • Neglect also happens for mental imagery and emotional content may implicitly affect behavior
      • Theory: right hemisphere damaged, left hemisphere takes over and receives all attention  over-focus of right visual field
      • Patients often have anosognosia

      Neglect is different from hemianopia (V1 damage). Difficult to differentiate though (but hemianopia patients often know something is wrong).

      Balint’s syndrome

      • Bilateral damage to dorsal posterior parietal cortex and lateral occipital cortex
      • Optic & oculomotor apraxia: motor (arm&gaze) guidance to objects is impaired
      • Simultanagnosia: difficulty handling two objects at a time

       

      Parietal lobe damage: deficits in attention and changing the allocation of attention

      Frontal lobe damage: deficits in control & initiating the changes in attention

      Frontalparietal network = attentional control

       

      There is first activity in frontal areas, then in parietal areas.

      • cue: frontal activity
      • reorienting: parietal activity

      The TPJ (temporo-parietal junction) is specifically important for bottom-up processing of attention.

       

      During visual search you use a lot of bottom-up attention.

      • Pop-out search: automatically grabs your attention
      • Conjunction: top-down attention. You have to steer your gaze

       

       

       

      When searching for something, you are always driven by both pop-out and conjunction search. Reorienting during both types of visual search is coded in the intraparietal sulcus (IPS).

      Default-mode network: active in rest. Decreased activity in the frontoparietal network means increased activity in the default-mode network (inverse coupling) --> Posterior cingulate cortex

      EEG reflects sleep stages:

      • Relaxed: alpha activity
      • Stage 1 – drowsy: theta activity
      • Stage 2-3 – sleep: theta/delta
      • Stage 4 – deep sleep: delta
      • REM sleep: rapid eye movements

       

      Sleep neurotransmitters:

      • Acetylcholine – memory consolidation
        • Nucleus basalis
      • Noradrenaline / Norepinephrine – arousal
        • Locus Coeruleus
      • Serotonin --> melatonin – motivation, sleep onset, internal clock
        • Raphe nuclei, pineal gland
      • Histamine – vigilance, alertness
        • Hypothalamus
      • Orexin/hypocretin – stable sleep, appetite
        • Hypothalamus
      • Cortisol – awakening response
        • Pituitary gland
      • Glutamate – GABA (sleep
      .....read more
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      Lecture 7 - Memory: varieties & mechanisms (Cognitive Neuroscience, UU)

      Lecture 7 - Memory: varieties & mechanisms (Cognitive Neuroscience, UU)

      Representations: somehow the world is represented in the mind and the brain.

      Churchland & Sejnowski: the defining function of nervous systems is representational.

      Stored representations are believed to depend on the configuration of weights between units. In neural terms, these weights are the strength of synaptic connections between neurons.

      Some memory functions are intact in amnesic patients.

      • The declarative memory is impaired --> specific events
      • Procedural memory often intact --> skills

       

       

       

       

       

      Non-declarative (implicit) memory: memory without awareness. Skill learning, priming, classical conditioning.

      Priming tests consist of:

      • Free recall
      • Cued recall
      • Completion

      Classical conditioning: before conditioning, the animal responds to the US, but not to the CS. At this stage, this is called the unconditioned response or UCR. During the conditioning the CS and the US are paired repeatedly. Conditioning leads to a conditioned response.

      Delay vs trace conditioning in amnesic patients

      • Delay: involve procedural memory, is not impaired in amnesic patients
      • Trace: declarative memory; awareness, is impaired in amnesic patients

      Anterograde amnesia: amnesia for events after the trauma

      Retrograde amnesia: amnesia for events before trauma

       

      Hebb: there is simultaneous activity in two neurons.

      Changes in the effectiveness of synaptic transmission take place as a result of simultaneous pre- and postsynaptic activity.

      There are two research strategies for neurobiology of learning and memory:

      1. Top-down: presupposing a certain principle
      2. Bottom-up: no presuppositions about the mechanism, but attempts at localization.

      Top-down approach of LTP (long term potentiation) and memory.

      • LTP: single stimulation of perforant path fibres to dentate gyrus results in an EPSP.
      • After a brief tetanus (high frequent pulse; 250 Hz) the characteristics of the EPSP have changed.

      NMDA receptor: neurotransmitter can bind to this. But there is a (Magnesium) block. This can be removed by depolarizing the cell. So it requires two simultaneous events: 1. Depolarization 2. Glutamate in the cleft.

      Bottom-up approach: imprinting. The formation of early social preference for the mother or another stimulus.

      Memory formation involved structural changes in the connections between neurons. Such structural changes involve protein synthesis.

      Conclusions:

      • Brain damage (MTL) causes amnesia
      • Lead to distinction between different kinds of memory, incl. declarative memory and procedural memory
      • A number of different brain structures are involved in human memory
      • There are top-down and bottom-up approaches
      • Bottom-up has the best prospects for localization of the neural substrate for memory
      • Memory formation involves structural changes at the level of the synapse

      Questions? Let me know in the contribution section!

      Follow me for more summaries / lecture notes!

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      Lecture 8 - Declarative memory (Cognitive Neuroscience, UU)

      Lecture 8 - Declarative memory (Cognitive Neuroscience, UU)

      The hippocampus plays a big role in declarative memory: it is the ‘hub’ of memory.

      Medial temporal lobe lesions lead to severe and global amnesia. Remote memories are spared after MTL lesions.

      Within the hippocampus, there is spatial encoding by place cells.

      • Relation memory theory
      • Episodic memory theory

      Recollection: hippocampus

      Familiarity: perirhinal cortex

       

      Three-process theory of medial temporal lobe functions:

      1. Perirhinal cortex: object encoding
      2. Parahippocampal cortex: spatial layout encoding
      3. Hippocampus: fuses these aspects

      Semantic knowledge in the brain:

      • Sensory / functional theory
      • Domain-specific theory

      Semantic dementia: semantic memory loss due to dementia. Damage to the temporal cortex

      [note: deze afbeelding uit het college is door de WorldSupporter redactie verwijderd wegens vermoedelijke inbreuk op het auteursrecht] 

      Distributed-only view & Distributed-plus-hub view are two models of the cortical semantic network.

      There is a lot of evidence for the distributed-plus-hub view.

      Memories can become independent (outside of hippocampus).

      How are retrieval memories reactivated and becoming available again? So how are episodic memories reactivated?

      • Pair recall neurons reactivate the memory (increased activity)

       

      Role prefrontal cortex --> different parts are active for semantic and phonological pairs of words.

      Damage to frontal lobe lesions: source errors.

      Multiple trace theory of consolidation: hippocampus is always involved, and has multiple memory traces  explanation of complete retrograde amnesia.

      Memory is consolidated during sleep.

      Filial imprinting – the formation (through learning) of an early social preference for the mother or another stimulus.

      You need to sleep fairly soon after the learning experience for it to enhance memory.

      Conclusions:

      • Damage to the MTL causes amnesia: declarative memory
      • Declarative memory involved episodic (HPC) and semantic memory (anterior temporal lobe).
      • Three-process model of MTL
      • Semantic memory is about concepts (hub)
      • Involves a ‘hub’ in the anterior temporal lobe
      • Frontal cortex is involved in memory encoding and retrieval
      • Declarative memory is consolidated over time and involves sleep

      Questions? Let me know in the contribution section!

      Follow me for more summaries / lecture notes!

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      Lecture 9 - Emotion (Cognitive Neuroscience, UU)

      Lecture 9 - Emotion (Cognitive Neuroscience, UU)

      Emotion has a signaling function, for example for a threat to integrity.

      Emotions trigger adaptive responses. From evolutionary perspective: we use it for responses that are adaptive.

      Emotions are universal, the basic emotions are: happiness, surprise, fear, anger, disgust and sadness.

      • Primary reinforcers: satisfy for example hunger, thirst and safety
      • Secondary reinforcers: money, social recognition

      3 biosystems from evolutionary perspective:

      1. Reptilian brain: life support system, reflexive behavior
      2. Paleomammalian: motivation / emotion
      3. Neomammalian: higher level control

      Limbic system = the emotional brain.

      ANS controls the involuntary muscles.

      When you encounter a threat, your autonomic nervous system responds:

      • Sympathetic: fight / flight
      • Parasympathetic: rest & digest

      Hormones: HPA-axis. Releases glucocorticoids, which regulates stress.

      Fear response: LeDoux model. The amygdala is the important structure. He proposed there are different routes, a fast route and a slow route.

      The information enters the BLA (basolateral) amygdala. Then projections are sent to the central amygdala, from where the projections run to the (hypo)thalamus.

      ‘Emotion’ areas of PFC:

      • Anterior cingulate cortex (ACC)
      • Subgenual subdivision of ACC (vmPFC)
      • Orbitofrontal cortex

       

       

       

       

      Amygdala is involved in fear conditioning.

      The CS will elict conditioned (fear) response:

      • Yes, with intact amygdala + startle
      • With skin conductance: only if learning takes place

      The ACC and the anterior insula are consistently activated in response to threat.

      In a study, no constant amygdala activation was found during fear. Why?

      • FMRI resolution too low (amygdala contains different, quite small areas)
      • FMRI time course (typically modelled as same response to each trial, whereas conditioning is a learning process that develops over time)
      • Human fear conditioning is only mild threat

       

      A fearful expression will slow down the reaction time in a stroop task. Also when the face is masked and the face is no longer recognizable.

      There is no amygdala activation when the attention to the fearful stimulus was explicitely directed away.

      There is no anatomical evidence for the fast route of LeDoux. There is however some evidence, such as affective blindsight, binocular rivalry.

      Evidence that non-attended or unconsciously processed information can activate amygdala does not necessarily mean that this information has been processed (exclusively) through subcortical channels.

      There should also be focus on networks, not only on isolated brain areas. Such as the salience network.

      Summary:

      • Emotion is an important driver of behavior
      • There are several levels of neural system involved in
        • Generating emotional response
        • Learning adaptive responses
        • Interactions between emotion and cognition
        • Responses are regulated through mutual connectivity

      Questions? Let me know in the contribution

      .....read more
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      Lecture 10 - Social cognition (Cognitive Neuroscience, UU)

      Lecture 10 - Social cognition (Cognitive Neuroscience, UU)

      Our brains may have grown in size because we are social animals.

      The orbitofrontal cortex plays a role in social functioning.

      • OFC damage: over-reliance on perceptual cues to guide behavior
      • Difficulty placing appropriateness of behavior in context
      • Lack awareness of whether their own/other’s behavior is appropriate

      Somatic marker hypothesis

      • Fast activation of ANS by affective associations: somatic states are induced
      • Potential threats or rewards are signaled before conscious knowledge of such a threat / reward
      • Sort through behavioral options to limit choice

      vmOFC: associates a ‘gut-feeling’ with each choice – helps sort through available options.

      Patients with vmOFC damage: the somatic marker does not cause the SCR reflects to be a learned association.

      The somatic marker occurs when you’re about to do something risky.

      The default mode network may be involved in self-referential processing.

      Most people think they are better than average: the better than average effect.

      • More medial and lateral OFC recruitment leads to more realistic evaluations of self compared to others.

       

      Processing others’ thoughts (theory of mind) can be measured using the false-belief test.

      The TPJ is specifically involved in processing stories on other people’s thoughts. Why is this active?

      • Role: enables shifts of attention
      • In vision: attention shifts to other locations
      • Hypothesis: TPJ enables shifts of attention to other viewpoints in social reasoning.

      Mirror neurons and mimicry also play a role.

      These mechanisms may be deficient in autism. For example, the higher the autism quotient, the lower the mimicry.

      People with autism look at the eyes way less than healthy controls.

      High testosterone prenatally: low scores on the reading the eyes in the mind task.

      Oxytocin: bonding hormone. Oxytocin enhances fixations on eye region and improves reading mind from eye.

      Summary:

       

       

       

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      Lecture 11 - Language (Cognitive Neuroscience, UU)

      Lecture 11 - Language (Cognitive Neuroscience, UU)

      Phonology: the study of the abstract sound patterns of a particular language, usually according to some system of rules.

      Syntax: the rules for arranging items into their possible permissible combinations in a language.

      Semantics: the analysis of the meaning of a language.

      Language is a system of discrete infinity. There is a finite number of elements, but unbounded use of those elements.

      Human language is grounded on a particular computational mechanism, realized neurally. Each expression is assigned an interpretation at two interfaces.

      There is a sensitive period for learning a 2nd language:

       

       

       

       

      Language wars:

      • Language involves Universal Grammer
      • Language acquisition is usage-based through statistical learning.

      Language has a hierarchical structure.

      Aphasia: an impairment in language understanding and/or production that is caused by brain injury.

      Damage to Broca’s area and Wernicke’s area is different and expresses itself differently. The damage is always on the left side of the brain, because language is lateralized.

      Late 20th century view:

      • Broca’s area: syntax
      • Wernicke’s area: lexicon

      Contemporary view:

      There are two networks; in the frontal and temporal lobes. They interact all the time. There are interactions through dorsal and to ventral pathways.

      Neural mechanisms for syntax and hierarchical structures

      • Assembly of hierarchical structures involves Broca’s area
      • Complex sentence proceeding involves VA 44 and STC via their dorsal connection
      • STC supports integration of syntactic and semantic information to achieve sentence interpretation
      • STS-PMC connection is present at birth and supports auditory-based phonological learning, but NOT complex syntax

      Newborn’s Wernicke’s area is not yet connected to Broca’s area. But it is connected to the premotor cortex.

      So there is a sensory-to-motor mapping system. And there is a dorsal system (syntax, hierarchical structures) and ventral system (processing of semantic information.

      Ability to imitate sounds is necessary for language in humans. Not in monkeys.

      Convergence: different species have come up with similar solutions for similar problems.

      2 month old infants: the brain responds more to the sound of the mother than a stranger (is related to memory).

      FOXP2 gene mutation causes aphasia to develop. Other animals can have this mutation as well. It is however not a language gene, because:

      • Genes make proteins, not behavior
      • FOXP2 affects other genes
      • Whatever effect it has is in combination with numerous other genes
      • Mutation has multiple effects, not only on speech.

      Conclusions:

      • Language is not the same ass peech or communication
      • Language is a computational system, in the mind
      • Broca’s & Wernicke’s area / aphasia
      • Language is lateralized neurally
      • It involved complex interactions between frontal and temporal networks
      • Language likely evolved very recently, only in
      .....read more
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      Lecture 12 - Executive Function (Cognitive Neuroscience, UU)
      Lecture 13 - Decision making (Cognitive Neuroscience, UU)

      Lecture 13 - Decision making (Cognitive Neuroscience, UU)

      Utility: psychological value assigned to an outcome.

      Prospect theory

      • Prospect: option whose future rewards and probabilities are known or can be estimated.
      • It is a descriptive theory: it describes what people will choose instead of should do.
      • It differs from the expected-utility theory in two ways:
        • Reference dependence: current state is a reference point
          • Reference point
          • Diminished sensitivity
          • Loss aversion
        • Probability weighting: subjective perception of probabilities
          • Possibility effect: a chance is better than no chance
          • Certainty effect: no risk is better than some risk

       

       

      Primary reinforcer: rewards that have a direct benefit for fitness

      Secondary reinforcer: neutral outcome that has been turned into a positive one

       

      Substantial nigra and ventral tegmental area are the dopamine nuclei.

      In rats, the dopaminergic system was removed, and the rats still liked certain tastes. This indicates wanting instead of liking: motivation to pursue a reward.

      Nucleus accumbens: activated by wide range of motivationally relevant stimuli. Reinforcement of a desirable association.

      DA neurons signal changes in information:

      Reward prediction error (RPE): the actual outcome differs from what was expected.

      Actor-critic models: the brain has 2 systems

      1. Critic: evaluation, are rewards better or worse than expected?  ventral striatum (RPE)
      2. Actor: updates values of potential courses of action  dorsal striatum

      Damage to reward pathways:

      • Motor: Parkinson’s, Huntington’s
      • Psychiatric: schizophrenia, depression, ADHD

      Pathological gamblers’ brains ‘learn’ from near-misses. Males 14-22 years old, prefrontal cortex not fully developed yet.

      Salience can lead to dopaminergic increase.

      Uncertainty: psychological state of having a lack of information.

      Risk: decision has multiple potential outcomes with known probabilities

      Brain regions risk taking:

      [note: deze afbeelding uit het college is door de WorldSupporter redactie verwijderd wegens vermoedelijke inbreuk op het auteursrecht] 

      Ambiguity: probabilities of the outcomes cannot be known. OFC and PFC are involved.

      Dual system: two separate processes

      • Kahneman:
        • System 1: fast, parallel, automatic, context-dependent
        • System 2: slower, serial, controlled, evidence-based

      Social stimuli are rewarding. How rewarding depends on the social relationship.

      Two theories:

      1. Motivated by internal, reinforcing reward signals
      2. Required social cognition to recognize another individual’s needs

      Parietal cortex: social cognition

      mPFC: thinking about other people’s mental states

       

      Game theory studies how decisions are made in complex situations.

      • Prisoner’s dilemma
      • Ultimatum game
      • Trust game

      Altruistic punishment: censuring people who violate social norms.

      Currency signal: neurons tracking subjective value, regardless of category.

      Drift-diffusion models: assume that decision making is a random drift from neural states towards thresholds for action.

      Modality-indepenent value signals:

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      Lecture 14 - Evolution (Cognitive Neuroscience, UU)

      Lecture 14 - Evolution (Cognitive Neuroscience, UU)

      Development of traits:

      • Variation
      • Heritability
      • Natural selection / adaptedness

      Key factor is selection pressure

      Are we dealing with common descent or with convergence?

      • Common descent: we lijken meet op apen omdat deze dichterbij liggen in de evolutie
      • Convergence: unrelated species have come up with similar solutions to similar problems

       

      • Homology: a trait is of common descent
      • Analogy: a trait is functionally similar but was not derived from the same ancestor

      False dichotomies in evolution studies:

      • Innate – acquired/learned
      • Genes – environment
      • Instinct – learning
      • Nature – nurture

      What is innate? Different opinions:

      • Present at birth
      • Behavioural difference caused by a genetic difference
      • Adapted over the course of evolution
      • Unchanging throughout development
      • Shared by all members of a species
      • Present before the behavior serves any function
      • Not learned

      Lorenz: behavior can be dissected in innate and acquired/learned components.

      • Animals reared in complete isolation would show behavior that is completely innate, = Kaspar Hauser experiment

      Lehrman: behavior is the result of a complex interaction between the individual and its internal and external environment.

      No new neurons are generated after birth.

      At birth there are (too) many synaptic connections, so pruning takes place.

      Does absolute size matter? No, if the body is bigger, the brain is too. So look at relative size.

      Cortex size does matter. Forebrain complexity is characterized by cell groups.

      Brains tend to get bigger and bigger. Why? 3 hypotheses:

      1. Foraging hypothesis: differences in brain size are due to differences in the way animals get their food.
      2. Social intelligence hypothesis: the more social interactions are needed (larger social group), the larger the brain (relatively).
      3. General intelligence hypothesis: species differences in social learning and innovation are linked to brain volume.

      Group size does not covary with primate general intelligence score.

      Summary:

      • Cognitive traits covary together in primates, raising the possibility of a primate general intelligence, that includes elements of social intelligence
      • The g measure covaries with brain volume measures but not group size
      • High g species appear in several groups, suggesting independent evolutionary events
      • Conserved general processes, as opposed to specialized modules, may be an important part of primate cognitive evolution and the evolution of social learning

      Misinterpretations of the view of evolution:

      1. Medieval view of evolution (scala naturae)
        1. Scant consolation
        2. There is no cognitive scaling in nature
      2. Confounding evolution and mechanism
        1. Tinbergen’s 4 why’s regarding behavior: evolution, function, development, mechanism (causation).
        2. Adaptive specialisations: the whiskers of a bunny are well represented in the brain
        3. Based on food storing birds: it is
      .....read more
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