Lecture 4: Hormones & Behavior (NSBED, UU)

Steroids hormones such as estradiol, cortisol and testosterone are important in social emotional behavior. It seems that the estrogen line developed 100 mya earlier than the male androgen line.

 

The sex steroids testosterone and estradiol are the playmakers.

The social peptides vasopressin (AVP) and oxytocin are the goalgetters.

 

T underlies the gene expression of AVP (male type line).

E underlies the gene expression of oxytocin (female type line).

Note that female/male type is not female/male (T converts into E).

 

The social condition in males decides whether testosterone is converted into estradiol.

Testosterone induces social dominance and fearlessness in male and female animals and humans. The effects of oxytocin depend more on species, sex and personality.

Testosterone does not cause aggression by itself. Conditions have to be met for aggression to be provoked.

Low status threat: testosterone upregulates dopamine action in the OFC, which induces decoupling of the OFC and amygdala.

High status threat: in addition to the decoupling, testosterone upregulates AVP expression in the amygdala, this induces hypocoupling. 

 

Testosterone --> specific social fear

Oxytocin --> generalized anxiety

 

Oxytocin is thought to be the ‘good hormone’ and T the ‘bad hormone’, but scientific research suggests differently.

Oxytocin makes you love your in-group more, but not your out-group.

 

Emotion recognition: the orbitofrontal-amygdaloid circuit: for threat faces; the OFC reads-out the amygdala. Testosterone decreased angry faces recognition. Oxytocin increases facial mimicry. Several functional and structural MRI studies show involvement of the inferior frontal gyrus in mind-reading. Testosterone decreases IFG connectivity.

Oxytocin reduces pain, and empathy for pain.

So:

T impairs / OXT improves cognitive empathy and decreased empathic mimicking

OXT decreases empathy for pain / T we show no effect on empathy for pain.

Hypothetical model of the hormones / social brain:

 

 

 

 

 

 

Questions? Let me know in the contribution section!

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Neuroscience of Social Behavior and Emotional Disorders (NSBED) - Lectures (Universiteit Utrecht)

Lecture 1: Introduction & Methods (NSBED, UU)

Lecture 1: Introduction & Methods (NSBED, UU)

Social neuroscience is a combination of sociology, psychology and neuroscience.

The social brain is non-modular: social behavior is the result of a network.

Evolution of social (and non-social) behavior:

  • Bigger brains lead to changes in both social and non-social intelligence
  • Alternative (social intelligence hypothesis): social pressure to outwit peers may lead to increased intelligence in social and non-social domains.

Triune brain model: the human brain is an accumulation of brain regions that can be roughly divided in three phylogenetic stages:

  • The reptilian brain (sub-cortex)
    • Action-reaction machinery
  • The mammalian brain (limbic system)
    • Emotionality: behavioral flexibility
  • The primate brain (neo-cortex)
    • Rationality: the behavioral control

 

 

 

 

Sometimes a part of our behavior is still driven by similar brain mechanisms.

Reptilian brain: quite modular. Consists of small nuclei with distinct (non)social roles.

Mammalian brain: module-like. Amygdala/insula – fear/disgust

The primate brain: non-modular. But: mirror neurons.

Mirror neurons: neurons that respond to both self-behavior and other-behavior. Thought to serve observational learning. Are not tightly localized to one region.

Conclusion: the social brain might be a mixed mode of modularity.

Psychological methods in which we can measure behavioral and cognitive measures

Subjective measures

  • Emotional experience (interview or POMS)
  • Personality questionaires (e.g. STAI/STAS)
  • Use it for:
    • Control variable
    • Correlation with other measure
    • To compare different studies

Observational measures

  • What will the participant do?
  • But also eye tracking

Performance measures

  • Speed and accuracy
  • IQ tests
  • Recognition tests
  • Selective attention

Phychophysiology --> controlled by the brain through the spinal cord. ((Para)sympathetic nervous systems). 

Physiological methods

  • Skin conductance (sweat gland activity)
  • Heart rate, respiration (preparation for fight/flight
  • Electromyography (EMG; muscle activity)

Skin conductance (SCR)

  • You measure sweat gland activity
  • Peak between 1-5s

Heart rate

  • Deceleration: preparing for danger
  • Acceleration: active escape or attack
  • Heart rate variability (HRV)
    • More variability = rest = parasympathetic
    • Less = concentration, enhanced attention = sympathetic

Electromyography (EMG)

  • Measures potential between pairs of close elektrodes
  • Muscle activity
  • Application:
    • Mimicking facial expressions (affective empathy)
    • Startle potentiation

Brain imaging methods

  1. Electrophysiology
  • Single-cell recordings
  • Electroencephalography (EEG)
    • Possible to the column-like organization of the cortex (therefore also limited to the cortex)
    • Frequency bands approach
      • Delta-waves (1-4 Hz): motivational system (bottom-up drive)
      • Beta-waves (12-30 Hz): cortex: top-down modulation
    • Event-related
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Lecture 2: Evolution, Emotion & Motivation (NSBED, UU)

Lecture 2: Evolution, Emotion & Motivation (NSBED, UU)

When talking about emotions, it’s important to not only talk about electrical connections, but also chemical connections: neurotransmitters.

  1. Glutamate (excitatory)
  2. GABA (inhibitory)

These cause synaptic transmissions.

Neurotransmitters relating strongly to emotion:

  • Norepinephrine (noradrenalin)
    • Locus Coeruleus: fight-flight / arousal
  • Serotonin
    • Raphe nuclei: mood / impulsivity
  • Dopamine
    • Ventral tegmental area: Mo(tiva)tion / reward

These are neuromodulators: made in the brainstem and then transported to other parts in the brain, where they are released and influence the synaptic transmissions (G&G).

Neuropeptides are a different type of neuromodulators. Are produced in the pituitary gland, based on signaling from the hypothalamus. So: hypothalamus > pituitary > peptide > emotion:

  • Opioids (endorphins)
    • Pleasure
    • Motivation
  • Vasopressin
    • Social aggression
  • Oxytocin
    • Maternal bonding

Steroid hormones are also neuromodulators. Hypothalamus > pituitary gland sends precursors > body > hormones > emotion.

  • Testosterone
    • HPG axis
    • Social aggression
    • Sex
  • Cortisol
    • HPA axis
    • Fear
    • Arousal

Cognition is in the brain, and emotion in the body.

The hypothalamus directly coordinates the autonomous nervous system (ANS; parasympathetic and sympathetic nervous system).

The autonomous nervous system is part of the reptilian complex (approach / avoidance system. Behavior based on reactivity.

The paleomammalian complex/limbic system contains the:

  • Hypothalamus (control of ANS and hormones)
  • Striatum (reward, joy)
  • Amygdala (fear)
  • Insula (disgust)
  • Hippocampus (memory)

Behavior is based on attention and conditioning.

The neommalian complex/neocortex: behavior based on subjective / affective experience, social interaction and ratio.

Motivation: states in which rewards are sought and punishers are avoided (approach / avoidance (action based))

Emotion: states associated with stimuli that are rewarding and punishing (liking / disliking (subjective)):

  • Emotional reacting: acute state in response to something (surprised)
  • Emotional feeling: the subjective experience of emotions (joy)
  • Emotional mood: a diffuse affective state that is often of lower intensity than emotion but considerably longer in duration (happiness)

We have the physical ‘arousal’ caused by the ANS, and we have the mental experience that comes with it.

  • James-Lange theory: Event > arousal > experience. But: arousal doesn’t always lead to the same experience.
  • Reversed in Cannon-Bard theory: arousal after experience. But: we can experience arousal without any conscious recollection why.
  • Papez & Maclean: Event > independent arousal and experience. However, the brain has a lot of connections so it is unlikely that it is fully independent.
  • Schachter & Singer: event > (arousal + interpretation) > experience. ButL some emotional experience exist without interpretation.
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Lecture 3: Socio-Emotional Disorders (NSBED, UU)

Lecture 3: Socio-Emotional Disorders (NSBED, UU)

Highlights of paper by Porcelli et al.:

  • The human brain shows levels of specialization for social stimuli processing
  • Social brain could be affected by several psychiatric disorders
  • Mechanisms underlying social dysfunction are largely similar across disorders
  • Social dysfunction and social withdrawal may represent a transdiagnostic domain

The core message: complex social environments were a selective pressure for the human brain. This high complexity is associated with a high susceptibility to social psychopathology.

Social deficits can be the first signs of a ‘non-social’ psychiatric disorder.

In one sentence: the article provides neurobiological substrates of how in 3 frequent disorders (AD, SCZ and MDD) similar maladaptive mechanisms underlie social withdrawal.

There is dense white matter tract between the orbitofrontal cortex and the amygdala. This tract has been linked to a range of social disorders.

There are five large-scale brain networks for social behavior:

Amygdala networks:

  • Perception network
  • Affiliation network
  • Aversion network

Non-amygdala networks:

  • Mentalizing network
  • Mirror network

What you need to know:

Social perception: detection and processing of social stimuli:

  • Amygdala is the hub in the face processing network, involving the
    • Fusiform face area
    • Posterior STS
    • Occipital face area

Social affiliation network:

  • Role: to form and maintain social bonds
  • Ventromedial PFC, ACC and medial temporal cortices

Emotion regulation:

  • Amygdala is connected to vmPFC
  • Increased functional couplic is related to increased ability of emotion regulation

Social aversion network:

  • Amygdala is hub
  • ACC, insula and connectional targets in striatum, hypothalamus and brainstem.

Mirror network:

  • Selection of temporal, parietal and sensory motor brain regions

Mentalizing network:

  • ACC, mPFC, inferior frontal gyrus and temporopartietal junction
  • Is decomposed into:
    • Dorsal subnetwork: abstract third-person (others) information
    • Ventral subnetwork: engages when embodies first-person information is required.

Social functioning is highly impaired in AD, SCZ and MDD. All groups show a reduction in social connections.

Part 2: neuro-evolutionary model of depression

Adaptive functions of depression (or low mood):

  • Communicating a need for help
  • Saving valuable resources
  • Giving up commitment to unreachable goals

According to some scientists, pessimism and lack of motivation inherent to depression, or low mood, give a fitness advantage by preventing actions which led to nothing. The ability to feel bad and do nothing about it is an adaption.

Active coping: sympathetic activation

Passive coping: parasympathetic activation

Passive coping strategies, such as social withdrawal, can result in clinical depression.

Conservation withdrawal response (passive coping) started by e.g. jawless armoured fish: because they only use the parasympathetic system. Timeline:

450 myo: jawless armoured fish with only parasympatethic system

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Lecture 4: Hormones & Behavior (NSBED, UU)

Lecture 4: Hormones & Behavior (NSBED, UU)

Steroids hormones such as estradiol, cortisol and testosterone are important in social emotional behavior. It seems that the estrogen line developed 100 mya earlier than the male androgen line.

 

The sex steroids testosterone and estradiol are the playmakers.

The social peptides vasopressin (AVP) and oxytocin are the goalgetters.

 

T underlies the gene expression of AVP (male type line).

E underlies the gene expression of oxytocin (female type line).

Note that female/male type is not female/male (T converts into E).

 

The social condition in males decides whether testosterone is converted into estradiol.

Testosterone induces social dominance and fearlessness in male and female animals and humans. The effects of oxytocin depend more on species, sex and personality.

Testosterone does not cause aggression by itself. Conditions have to be met for aggression to be provoked.

Low status threat: testosterone upregulates dopamine action in the OFC, which induces decoupling of the OFC and amygdala.

High status threat: in addition to the decoupling, testosterone upregulates AVP expression in the amygdala, this induces hypocoupling. 

 

Testosterone --> specific social fear

Oxytocin --> generalized anxiety

 

Oxytocin is thought to be the ‘good hormone’ and T the ‘bad hormone’, but scientific research suggests differently.

Oxytocin makes you love your in-group more, but not your out-group.

 

Emotion recognition: the orbitofrontal-amygdaloid circuit: for threat faces; the OFC reads-out the amygdala. Testosterone decreased angry faces recognition. Oxytocin increases facial mimicry. Several functional and structural MRI studies show involvement of the inferior frontal gyrus in mind-reading. Testosterone decreases IFG connectivity.

Oxytocin reduces pain, and empathy for pain.

So:

T impairs / OXT improves cognitive empathy and decreased empathic mimicking

OXT decreases empathy for pain / T we show no effect on empathy for pain.

Hypothetical model of the hormones / social brain:

 

 

 

 

 

 

Questions? Let me know in the contribution section!

Follow me for more summaries / lecture notes!

Access: 
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Lecture 5: Faces and bodies (NSBED, UU)

Lecture 5: Faces and bodies (NSBED, UU)

Social Intelligence hypothesis: to outsmart the other, stronger animals, humans have to join forces. The ability to understand and predict complex social interactions is the main pressure for human intellectual development.

 

According to Haxby’s model of face encoding, you can divide a core system and an extended system:

  • Core: coding of basic features that constitute a face
  • Extended: cognitive and higher order processing such as emotions and biographic information.

Fusiform face area: located in the ventral stream on the ventral surface of the temporal lobe on the lateral side of the fusiform gyrus.

It takes 170 seconds for a person to recognize a face as a face (see picture).

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

 

The structural encoding of the face features is suggested to be separate from the processing of the emotional content.

There is increasing evidence that the cerebellum is involved in implicit and explicit cognitive processing of emotional faces.

When looking at threatful faces, the excitability of the motor cortex increases and it takes less effort to make a movement. 

Mimicking: as response to a negative emotional face, you are tended to respond with a negative emotion.

Bodily posture is another important feature that we use to infer emotional states and intention of others.

Embodiment: putting oneself in the skin of others or empathy in its original meaning of perspective taking.

There are three circuits in emotional body language:

  1. Reflex-like emotional body language
  2. Body awareness of emotional body language
  3. Visuomotor perception of emotional body language: the system that makes the transition between the experience of the emotional body expression towards the action.

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

 

When looking at angry body postures, the excitability of the motor cortex increases and it takes less effort to make undertake action.

The cerebellum contributes to the understanding of emotional faces/postures and embodiment.

Take home message: the brain contains dedicated neural circuits associated with the processing of faces and bodies in support of non-verbal social communication, intentions of others and action selection.

 

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Lecture 6: Understanding others (NSBED, UU)

Lecture 6: Understanding others (NSBED, UU)

Simulation theory: we understand others by simulating their states and executing their actions --> simulation in service of action understanding, or perhaps the other way around?

But how do we perceive action?

  • We categorize behavior (context)
  • Traits and stereotypes
  • Goal inferences

Ideomotor action: thought leads to action

How does the mind move the body?

  • Basic action preparation: premotor cortex (PMC) and supplementary motor area (SMA)
  • Action execution: primary motor cortex (M1)

Motor programs guide our actions, but how do we know which programs to use?

  • Learning through trial and error
  • Theory of event coding: we represent and select actions in terms of their outcomes

So action-effect relations are learned. Actions are represented in terms of their effect. Thinking of an effect selects the corresponding motor pattern.

People control their actions because the representations for perception and action share common codes, that can be activated by seeing, thinking about or reading about other people’s actions or goals.

Mirror neurons: responded to the perception of action, but are also activated when doing the action yourself. Mirror neurons do not only react to the perceived action, but also to the goals of those actions. There is some evidence for mirror neurons in humans.

Cognitive empathy: understanding intentions, believes and mental states.

Affective empathy: understanding feelings, emotions and pain

There are areas of cognitive and affective empathy that overlap.

The Pinocchio Effect: the social Simon effect occurs for a real hand, but not for a wooden hand. But after watching the movie Pinocchio, the effects are the same as with humans.

Simon effect: there is a difference in accuracy or reaction time between congruent and incongruent trials.

There is evidence that complementary actions activate the mirror neuron system even more strongly.

So empathy and mirror neuron activation have something to do with each other. But how are they related and can empathy disorders such as autism be explained in terms of non-functioning mirror neurons? --> Children with autism are less able, or less motivated to mirror the actions that they see in front of them

So activation is dependent on motivation / capacity to understand others.

 

Conclusions:

  • We may rely on our own action representations to understand actions of others
  • However, simulation may be the result of action understanding rather than the other way around
  • Dependent on capacity / motivation

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Lecture 7: Olfactory Social Neuroscience (NSBED, UU)

Lecture 7: Olfactory Social Neuroscience (NSBED, UU)

We have this bias that smell is not important to us, probably because we find it hard to name them.

What’s remarkable about the smell brain autonomy?

  • There is limbic overlap, which is not surprising since smells can carry emotional value
  • Ipsilateral projection
  • No thalamic intermediary: the thalamus is processed without thalamic relay
  • Feedback to the bulb: top down modulation

We can quickly learn the importance of a smell.

Smell functions:

  • Judging whether food is edible
  • Avoid environmental hazards
  • Social communication

Summary part 1:

  • Human sense of smell is better than initually realized
  • Share smell skills with outher animals
  • Neuroanatomy: limbic (emotion), plastic (learning)
  • Social (sommunication) function

 

Humans seem to smell odors of fear and disgust following an all or nothing principle: they either smell it or they don’t (not quantified).

Damage in the amygdala stops odor-driven behavior, but leaves learned olfactory responses intact.

Summary part 2:

  • The smell of fear partially induces fear in a recipient: sender and receiver become on the same page
  • It biases perception, physiological and neural responses
  • Hardwired neural networks may be involved

 

Sickness affects your body odor.

There is a distinct network of regions activated when a person smells the body odor of a sick person.

Loss of smell is a better predictor of COVID-19 than fever+cough+shortness of breath.

Our ACE-2 receptors in the nose get infected by Covid-19.

High anxious subjects show a greater startle response to the smell of fear than non-anxious subjects.

ASD patients have more trouble detecting smells.

There have been found negative relations between psychopathic traits and smell ability. Lower smell ability has also been linked to low empathy.

Summary part 3:

  • Sickness affects your body odor
  • Smell loss is one of the best COVID-19 predictors
  • Psychopathology, hormones are related to smell ability
  • Trust your nose!

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Lecture 8: Interacting with Others (NSBED, UU)

Lecture 8: Interacting with Others (NSBED, UU)

Altruism: helping behavior that is considered selfless, there is no personal gain obtained and sometimes it is even costly to the helper.

What are the motives underlying helping?

  1. Intrinsic desire to help --> driven by prosocial motives such as empathy and fairness
  2. Benefits of reciprocity --> if I help you now, you might help me in the future
  3. Punishment for non-cooperation --> altruistic punishment
  4. Social conformity --> driven by the need to belong to a group

Evolutionary explanations for altruism:

  • Kin selection: we help our family
  • Reciprocal altruism: if I help you, you will help me in the future
  • Sexual selection: altruism as an attractive trait
  • Indirect reciprocity: helping people that you haven’t interacted with before and may never interact with again.

An individual motive can be empathy. Prosocial motives like empathic concern drives helping behavior. Three components of empathy:

  • Emotion contagion
    • facial mimicry can be measures with facial EMG
    • Mirror neurons
    • What is the goal of simulation? The relationship between helping and simulation is complex. Sympathize vs. personal distress
  • Empathic concern
    • Oxytocin; produced in the hypothalamus
  • Perspective-taking/mentalizing

So:

  • Helping could be motivated by:
    • Empathic concern & perspective taking
    • The need to reduce personal distress
  • Two routes to helping
    • Impulsive: based on ‘hunches’ (emotional impulses)
    • Cost-benefit analyses

There are also social forces that influence helping behavior. Donating is for example the more social desirable response. Social conformity is not to be confused with social obedience (e.g. Milgram’s studies). Asch experiment is an example of social conformity.

Psychopaths display the opposite neurocognitive pattern of extreme altruists.

Helping friends --> dorso-lateral prefrontal cortex  related to self regulating and strategic behavior

Helping strangers --> dorso-medial prefrontal cortex  cognitive empathy and mentalizing

Neuroeconomics: combines neuroscience and games to reveal neural systems underlying social decision making

Response to fair offers (controlled for the amount of money):

Afbeelding met tekst, taart, binnen

Automatisch gegenereerde beschrijving

 

 

 

Responses to unfair offers:

 

 

  • Fair offers and cooperation induce striatum responses (reward)
  • Unfair offers trigger insula response (disgust and anger)
  • DLPFC response (biasing towards fair behavior)

Take home message:

  • Humans make irrational decisions
  • Neuroeconomics has shown brain circuits involved in
    • Emotion: amygdala, insula
    • Valuation/reward: verntral striatum, OFC, ACC
    • Social cognition DMPFC
    • Self-regulation: DLPFC
  • Contextual factors might determine the relative contribution of these circuits

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Lecture 9: Relationships (NSBED, UU)

Lecture 9: Relationships (NSBED, UU)

What is a relationship? Just interaction is not enough. There has to be distress and longing in separation, and a sense of well-being in presence. Also known as social bonds.

Relationships have health benefits.

Love is the emotion associated with being in an attachment relationship.

Sternberg’s Triangular theory -  love consists of three factors:

  • Passion
  • Commitment
  • Intimacy

The passionate phase lasts 6 months to 3 years. Other factors may ensure continuation after this face (intimacy, cost of leaving, etc.). Arranged marriages are high on commitment, but other factors may increase over time.

Falling in love has similarities with clinical symptoms of for example OCD.

Hormonal and neurochemical changes are associated with only the passionate phase of a relationship.

 

  • There is activation of dopamine in the VTA when seeing photos of partner.
  • There is also activity in reward-related regions linked to oxytocin / vasopressin.
  • There is deactivation in regions such as amygdala, temporo-parietal junction, mPFC (mentalizing regions).

Love acts as a buffer against stress and pain.

Attachment is found in all animals in which infants are initially in need of care.

The brain area that is activated as response to infant faces is rich in oxytocin and dopamine. 

According to Ainsworth et al. (1978) there are three types of attachment that relate to different types of parental sensitivity:

  1. Secure                        -           Moderately upset at separation, greets positively
  2. Insecure anxious        -           Highly stressed at separation, hard to comfort at reunion
  3. Insecure avoidant      -           Avoids contact, especially at reunion

Attachment security predicts neural differences in face processing for infants and mothers.

Attachment insecurity increases SCR and amygdala activity.

Mother infant bonding forms the basis of other forms of social bonding. It is founded upon the same neural circuit.

Oxytocin is strongly related to maternal behavior.

Partner preference paradigm – disruption of oxytocin/vasopressin prevents partner preference formation.

Opioids – powerful painkillers and act on reward related mechanisms. It can upregulate the reward of social interactions and motivates us for it.

Panksepp’s brain opiod theory of social attachment – opioids contribute to emotional responding in close relationships and also to the behavior that might promote further bonding.

OXT promotes trust in humans. OXT administration results in increase in activation of the reward system when seeing pictures of partner. It reduces amygdala activation in response to fear stimuli

The effect oxytocin has on stress is modulated by the effect of oxytocin on the HPA axis.

So:

  • Mother infant bonding shared neural circuitry (mammals)
  • Forms the basis of other forms of social bonding
  • Which is founded upon the same neural circuitry
  • And neuro-endocrine system

Social pain may be evolutionary adapted from physical pain.

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Lecture 10: Groups and Identity (NSBED, UU)

Lecture 10: Groups and Identity (NSBED, UU)

Social categorization is visible in task performance.

There is a racial bias.

The brain has an automatic conflict-detection system, located in the ACC. It signals us when we are in conflict situations that require attention. You see the effect of an error:

 

 

 

 

The stronger the error detection, the less behavioral bias in shooter task.

People who are intrinsic motivated to respond without prejudice show stronger error detection. Extrinsic motivation doesn’t improve performance!

Within 200ms, the brain categorizes others around us in terms of race, gender, sexual orientation. This triggers implicit associations with ingroup (positive) and outgroup (negative), leading to bias in behavior.

It is possible to control these automatic biases by monitoring performance, detecting conflict between goals and failure to achieve these goals. However, for this you either need to be intrinsically motivated or reminded of your moral values.

The empathy gap – the empathy we feel for people like us is much larger than for people unlike us.

Mu suppression – indicates motor cortex activity. It can happen when you see other people move. Happens more when you see people of the ingroup than people of the outgroup.

Stronger activation in the anterior insula in pain of own race.

  • Empathy is based on neural simulation of actions (motor cortex) and emotions (anterior insula)
  • We are less likely to simulate the behaviors and emotions of outgroup members

Stereotype threat – when people are reminded of stereotypes about their group. This creates threat. This threat is cognitively distracting.

Biopsychosocial model of threat and challenge – two motivational states:

  1. Threat: cognitive appraisal of situation where demands exceed resources.
  2. Challenge: cognitive appraisal of situation where resources meet or exceed demands.

It uses the responses of the autonomous nervous system to determine threat and challenge.

 

 

 

​​​​​​​

  • Priming people with negative stereotypes about their group can damage their performance
  • Threat of negative stereotypes activates brain areas associated with emotion regulation and social concerns.

Social pain triggers a neural alarm system that consists of the dorsal ACC and rvPFC.

Repeated exposure to social pain increases sensitivity of neural alarm system: more vigilance for social pain and the pain becomes more intense. This also has negative health outcomes.

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