PSYC 304 - Emotion, Stress, Aggression

James-Lange theory

stimulus → physiological response → emotion

• emotions are a result of bodily changes

weakness of James-Lange theory

• no distinct, separate physiological repsponse for each emotion

• same autonomic change (eg: increased heart rate) can be linked to fear excitement, anticipation, more

Cannon-bard theory

stimulus → emotion + autonomic response simultaneously

• cerebral cortex decides emotion and triggers bodily changes at the same time

• allows cotext to shape your emotional interpretation of event

Schachter-Singer model

stimulus → autonomic arousal → cognitive appraisal → emotion

• physiogical arousal itself is non-specific, so emotional label depends on the environmental cues

experiment on Schachter-Singer model

• E injection, then exposure to either a happy or angry confederate

• participants reported their mood to match the confederate, especially when injected with E (compared to controls) so arousal was present

sympathetic nervous system

prepares body for action, eg: increased heart rate, dilated pupils

parasympathetic nervous system

promotes rest and recovery

amygdala effect on emotions

attaches emotional valence to the sensory input you receive, which links body arousal to context

low road of emotion

thalamus → amygdala for immediate, unconscious emotional reaction

high road of emotion

thalamus → cortex → amygdala for slower, conscious appraisal

PFC role in emotion

exerts top-down control, which modulates autonomic output

• eg: inhibiting fear when it’s not rationally necessary

branistem and hypothalamus role in emotions

regulate bodily functions such as heart rate and respiration, which are affected by emotional state

individual response stereotypy

• indivdiuals show consistent emotional reactivity patterns over their lifetimes

• infants being “high” vs “low” reactives tend to be stable going into adulthood

highly reactive individuals are more likely to develop…

anxiety, phobias, depression

temperament biases

• high reactivity = deeper processing of emotional cues

• socially anxious people respond more strongly to facial expressions

individual differences in emotions is influenced by…

• early environment

• genetics

• learned associations

Plutchik’s model of 8 basic emotions

• joy/sadness

• affection/disgust

• anger/fear

• expectation/surprise

Ekman’s facial expressions

anger, sadness, happiness, fear, disgust, surprise, contempt, embarassment

universality evidence for emotions

• many emotions are recognized across literate cultures

• non-literate cultures could consistently recognize happiness but not other emotions

• number of core emotions is debated, potentially depends on the number of facial expressions we can make

Darwin’s theory on emotions

emotional expressions are universal and shared with nonhuman primates

emotions effect on survival

aid by avoiding predators, choosing mates, cooperating in groups, securing resources

paralinguistic communication

conveying info to others without words

• eg: fearful expression warns others for survival

amygdala and Papez circuit function

evolved to detect threats and rewards quickly

facial expressions are controlled by which brain structures?

motor cortex and basal ganglia

facial expressions - regions involved

• supercficial and deep facial muscles

• facial and trigeminal cranial nerves

• motor cortex and basal ganglia

aggression

behaviour inntended to harm or assert dominance over another

proactive aggression

• goal-oriented and planned

  • eg: fighting for food, status, mating, etc.

reactive aggression

• emotional, defensive

  • eg: triggered by a perceived threat

adaptive benefits of aggression

• assert dominance and establish hierarchy

• defend resource/territory

• protect from predators

• hunt for survival

• posturing to avoid actual fighting

effects of T on animals

• increased intermale aggression at sexual maturity

• seasonal breeders increase aggression depending on season

• castration decreases aggression

• female hyenas have high androgen → more aggressive

fruit flies and aggression

does not depend on androgens, instead is linked to mating genes

effects of T on humans

link is weaker due to experience and dominance effects

experience effects of T

• winners have increased T, losers decrease

  • eg: their own games, favourite sports team, children’s teams

dominance effects of T

supports behaviour that gain and protect status, eg: prolonged eye contact with threats

serotonin effects on human aggression

low serotonin = high aggression

serotonin effects on animal aggression

• fruit flies: high serotonin = high aggression

• locusts: high serotonin = swarm/socialize together, despite being solitary insects

GABA effects on aggression

• enhancing GABA = less aggression

• the balance between GABA and glutamate is critical to regulate aggression

what other hormones can modulate social/aggressive tendencies?

vasopressin, oxytocin, endogenous opioids

medial amygdala - role in aggression

processes pheromonal cues, decides to approach or attack

ventromedial hypothalamus - role in aggression

triggers aggression in mice

• optogenetics: stimulation of this causes them to switch from mating to attacking

• inhibition of this brain region decreases male aggression

maternal aggression

strong during lactation, ventromedial hypothalamus is involved

Papez and limbic system circuit - role in aggression

emotional regulation and contextual memory (hippocampus, amygdala, fornix, cingulate cortex)

psychopathy

cluster of antisocial behaviours with emotional deficits

traits of psychopathy

• intelligence, superficial charm

• poor self-control and grandiose selfview

• lack of remorse/empathy

behavioural correlates of psychopathy

• blunted response to violence

• reduced fear conditioning

neurological correlates of psychopathy

• reduced size and activity in PFC, results in poor impulse control

• sometimes linked to temporal dysfunction = emotional dyscontrol syndrome

stress

anything that disrupts homeostasis

allostasis

ongoing adjustments to maintain stability in changing enviornments

alarm reaction (fight or flight)

• hypothalamus activates sympathetic NS

• adrenal medulla releases E, NE

• rapidly increases heart rate, breathing, blood flow to muscles to prepare body for action

endocrine pathway for stress

• hypothalamus → anterior pituitary → releasing hormones to trigger adrenal cortex, so it releases cortisol

• mobilizes stored energy and modulates immune response

acute stress

short-lived and adaptive to increase alertness and energy in survival situations

chronic stress

• prolonged cortisol elevation leads to negative effects

  • immune suppression, slower wound healing, hippocampal damage, cardiovascular strain

• humans have a unique capacity fro prolonged stress due to cognitive/social factors

stress immunization hypothesis

mild, early life stress + maternal comfort leads to greater resilience later in life

maternal deprivation results in…

long separation + low grooming → higher adult stress reactivity, poorer learning, decreased hippocampus neurogenesis

epigenetic regulation of stress

early adversity leads to reduced expression of glucocorticoid receptors in brain

evidence of stress immunization hypothesis

rat pups who are briefly handled (stressful scenario) have less adult stress reactivity when groomed right after

vulnerability factors of stress

• personality traits (eg: hostility, low social support)

• health behaviours (poor sleep, malnutrition, smoking)

• sense of purpose and motivation = protective factors

epigenetic effects on stress

• long-lasting changes to gene expression, without DNA sequence changes

• can persist into adulthood and potentially influence health decades later

negative early experiences - effcects on stress

downregulation of glucocorticoid receptors, meaning the body cannot process stress and is overwhelmed

phagocytes

engulf pathogens and debris, eg: macrophages, microglia

B lymphocytes

make antibodies against pathogens

T lymphocytes: types

• helper T cells

• killer T cells

helper T cells

make cytokines to activate immune system

killer T cells

destroy infected cells

microglia function

clear debris and mediate inflammation

• overactivation leads to too much inflammation, fatigue (brain fog)

effects of acute stress on immune system

cortisol suppresses inflammation, which is adaptive for fight-or-flight

• don’t want leg to swell when running away from predator

effects of chronic stress on immune system

immune suppression over time leads to higher infection risk and slower healing

bidirectional communication between brain and immune system

• brain detects immune activity (eg: how much cytokines)

• brain can suppress immune response by releasing ACh

• psychological cues (eg: seeing pics of sick people) can trigger cytokine release

dentist study

• lesioned mouth at beginning of year and at finals

• healing was slower during finals, about 40% due to suppressed immune system from stress

health risks of chronic stress

• increased risk of cardiovascular disease

  • especially when combined with hostility, type A personality risk factor

• immune suppression = higher rates

• slower wound healing