emotional behaviour Flashcards
limbic system
- includes forebrain area surrounding the thalamus
- critical for emotion
aggression: context dependent
depends on testing parameters
Sympathetic
stim organs for fight/flight (i.e. heart) inhibit vegetative activities (i.e. stomach)
- acute
Parasympathetic
increases digestion – save energy, prep for later events
Most situations invoke a combination of sympathetic & parasympathetic ie
become alert & inactive, heart rate decrease when danger is present but remote
physiological arousal & emotional feelings:
- spinal cord damage
- pure autonomic failure
- BOTOX blocking transmission at synapses (muscle paralyzation)
- Damaged right somatosensory cortex
- Partly damaged prefrontal cortex
- After damage to spinal cord – similar emotional experiences to before
- Pure autonomic failure: almost no output from autonomic nervous system to body
• No physiological reaction to stressful experience
• normal emotions reported – but less intense - Boltulinum toxin (BOTOX) blocks transmission at synapses & nerve-muscle junctions
• Muscles paralysed – weaker emotional responses - Damaged right somatosensory cortex: normal autonomic response, little subjective experience
- Partly damaged prefrontal cortex: weak auto response, normal subjective exp
- Sudden intense arousal of sympathetic NS without knowing the reason
may experience as emotion i.e. panic attack
- Physiological responses increase feelings (increase in HR – increase both pleasant & unpleasant)
“anger centre”??
doesn’t exist – certain patterns of activation are more closely associated to anger than sadness
- Much of the cerebral cortex reacts to emotional situations
- No brain area appears to be specific for experiencing any particular emotion
- Behavioural activation system
activity of frontal & temporal lobes of L hemi – low to mod auto arousal & approach
- Behavioural inhibition system
increased activity of frontal & temporal lobes in R hemi – increases attention, inhibits action, stim fear & disgust
aggression in hamasters (facing intrusion)
Home hamster facing intrusion:
- First attack of intruder: activity builds up in corticomedial area of amygdala (steroid sensitive)
• Increases probability of attacking the next intruder
- ## stained for an immediate-early gene: c-fos (cell nucleus)
orbital frontal cortex
inhibits action in medial amygdala
Aggressive, violent, antisocial behaviour depend on both environment & genes
- Env: childhood abuse, witness violent abuse b/w parents, live in violent neighbourhood, lead exposure
- Heredity : significant for aggressive behaviour but depend on how to measure
Genetic + environment effect on aggression: gene controlling enzyme monoamine oxidase A (MAO A) + bad environment
MAO A : an enzyme in synapse that breaks down/metabolize monoamines – some of serotonin/ dope/ norepi after reuptake
• Low activity (short form of gene) – less MAO A enzyme produced + bad childhood – link to aggression, less resilience (greater emotional reactivity?)
• Effect of gene depends on previous experience (increase aggression only in ppl with troubled childhood)
gene x env interaction
low serotonin (5HT) release (indicated by? & associated with?)
- Serotonin levels in neurons: fairly constant (neurons reabsorb most serotonin released & synthesize enough to replace the amt washed away)
measure instead: - serotonin metabolite levels (serotonin turnover) – concentration of 5-HIAA in extracellular space/ CSF - low metabolite levels associated with aggressive behvaiour & impulsiveness
- mice: social isolate increases aggression & decreases 5-HIAA levels)
twin aggression studies
mono twins resemble each other much more than dizygotic twins - violent & criminal behaviour
- adopted children resemble biological parents
humans – DHEA is inert
secreted by adrenals & converted into active sex steroids (T & E2)
- does not have its own receptors, not synthesized directly, antiglucocorticoid effects
hyp: same for T in song sparrows during non-breeding season? since T is not detected in blood plasma & gonads shrink
finding: enzyme 3 beta-HSD is upregulated in non-breeding season (increases capacity for local production of T), low in breeding season
hormonal effects on aggression
- Same age: those with higher T levels on avg tend to be more aggressive (both M & F)
• But differences are small
Hypothesis: aggressive behaviour depends on a sudden burst of T in response to an event (not baseline)
Testosterone, Serotonin & cortisol on agg behv.
- T (esp a burst of T) facilitates aggressive, assertive, dominant behaviour
- Ser tends to inhibit impulsive behv.
- Cortisol inhibits aggression (stronger than Ser)
- Adrenal gland: secretes cort during stress & anxiety – cautious behv conserves energy
anxiety &anger – effect on cortisol
anxiety increases Cortisol levels
- Anger decreases cort levels
- Both M & F: combination of high T & low cort increases aggressive & risky behv.
• Low cort: decreased fear of harmful consequences
• T: increases expected gain
Moro reflex in infants
sudden loud noise causes newborn arch back & cry
Startle reflex
loud noise – cochlear nucleus in medulla – area in pons that commands tensing muscles (esp neck) – in less than 2/10 of a second
• More vigorous if already tense
• Enhanced in ppl with PTSD/ more anxiety
can measure the startle reflex to measure anxiety
general adaptation syndrome
alarm stage: increased sympathetic nervous system activity (acute)
resistance stage: sympathetic response declines; adrenal cortex continues releasing corticosterone (rats) / cortisol & other hormones to promote alertness
exhaustion stage: occurs after chronic prolonged stress; insufficient energy to sustain responses
stressor
external stimuli
stress
internal perception of external stimuli
stress response
physiological responses to stressor
sympathetic NS vs HPA axis
SNS: fight/flight responses (acute transient stressors) vs HPA axis: activated under chronic, prolonged stressors
acute stress response
increased energy availability – blood glucose
increased oxygen intake
increased blood flow to muscles
inhibition of digestion, growth & repair , reproduction, pain perception
altered immune function (move to skin)
enhancement of memory & sensory info
adrenal medulla: secrete catecholamines (epinephrine, norepinephrine, dopamine ) – block receptors = decrease in BP
chronic stress response (repeated HPA axis stimulation)
can have pathological effects:
energy availability: type 2 diabetes mellitus
inhibition to reproduction: infertility
inhibition of growth & repair : psychosocial dwarfism, slower wound healing
inhibition of immune function: immunosuppression, impaired pathogen resistance
stimulation of CNS: neural degeneration
describe the HPA axis
responds to signals like elevated norepinephrine levels
hypothalamus secretes corticotropin releasing hormones (CRH) to anterior pituitary – (increases SNS activity) & A pit releases Adrenocorticotropic hormone (ACTH) into blood – reaches adrenal cortex –> releases glucocorticoids like Cortisol and DHEA
Cortisol: increases glucose levels by breaking down more glycogen (more energy available) – negative feedback to hypothalamus & A pit
DHEA: acts in opposition to CORT
hippocampus & stress
negative feedback to HPA axis
many glucocorticoid receptors (GR) – vs mineralocorticoid receptors (MR) : MR has higher affinity = baseline: lots of GR not bound – only bound when lots of GC present
prolonged high cortisol levels: dendritic atrophy of pyramidal cells & cell loss – vulnerable to overstimulation
hippocampal damage leads to increased cortisol levels (vicious cycle)
amygdala & fear
- Amygdala: important for enhancing startle reflex & learned fears
- Much input from sensory systems (vision, hearing) goes to lateral & basolateral areas of amygdala relay to central amygdala combines with pain & stress info received from thalamus
Mice with stronger connections b/w lateral & central amygdala: more anxious
• Fear learning: strengthens synapses at several connections
- A path through the amygdala for each fear: pain, predator etc
-
bed nucleus of the stria terminalis & fear
A set of axons that connect the bed nucleus to amygdala
– Long-term, generalized emotional arousal
re-appraisal
reinterpret a situation as less threatening *effective for coping
depend on top-down influences from prefrontal cortex to inhibit amygdala activity
ind differences in anxiety tendencies
- remain consistent over time for ppl
- variance: due to genes & epigenetic changes caused by early experiences
- ind differences correlate strongly with amygdala activity (biological predisposition)
Unipolar depression (major depressive disorder)
vary b/w normaliy & depression
- Feel sad & helpless most of the day every day for weeks at a time
- Nucleus accumbens becomes less responsive to reward
- Feel worthless, contemplate suicide, sleeping issues
- Cognitive problems: low motivation, impaired attention , memory & sense of smell
- Absence of happiness
- Common to have episodes of depression separated by normal periods
• FALSE: Early eps: longer; later: briefer but more frequent
risk factors: stress & inflammation : increased immune activity (i.e. after injury, highly stressful experiences)
lower levels of a neurotrophin
- Panic disorder
frequent periods of anxiety & occasional attacks of rapid breathing, increased HR, sweating, trembling – extreme arousal of Sympathetic NS
• Linked to abnormalities in hypothalamus
decreased GABA activity, increased orexin (drugs that block orexin receptors block panic responses)
- Post-traumatic stress disorder
frequent distressing recollections & nightmares of traumatic event, avoidance of reminders, vigorous reactions to stim
• Cannot be predicted based on severity of trauma / initial reaction intensity
• Most victims have a smaller hippocampus (increases susceptibility)
• Severe stress can impair function in the hippocampus (sometimes shrinkage)
• Recovery from PTSD does not increase size
behavioural tests in rats fro depressive-like behaviour
- forced swim test – latency to giving up
- lever press
- sucrose preference test : reduction in the sucrose preference ratio = more depressed
Relief from anxiety
Pharmalogical
- Anxiolytic (anti-anxiety) drugs: benzodiazepines, diazepam etc.
• Bind to GABA A receptor includes a site that binds GABA & sites that modify the sensitivity of GABA site - Chloride channel in GABAA receptor:
• Open: Cl- can enter neuron hyperpolarize cell/ counteract Na entering the cell through excitatory synapses (GABA synapse is inhibitory)
benzodiazepines twists the receptor so that the GABA binds more easily *facilitates effects of GABA
genetic predisposition to depression
Serotonin transporter (protein regulating axons’ reabsorption of serotonin) gene: • Ppl with 2 short forms of gene – stressful events led to major increase in risk of depression -- short form magnified reaction to stressful events (NOT Lead to depression) & increased emotional reactivity of any type
dexamethasone (DEX)
artificial steroid: high affinity for glucocorticoid receptors
- mimics GC binding & increase glucose levels
in normal control: result in decreased GC levels
in depressed patients: GC levels are still high
– DEX suppression test can be potentially used for diagnosis
non specific (innate) immunity
rapid first line of defence monocytes & macrophages
destroy anything “non-self” – but can also damage self
specific (adaptive) immunity
slower
cell-mediated: T cells (lymphocytes) – mature in thymus: attack pathogens directly (cytotoxic T cells) & help other T & B cells to multiply (helper T cells)
kills specific pathogen upon re exposure
cytokines
small proteins produced by leukocytes & others
- combat infection & inform brain
- stim release of prostaglandins – fever & sleepiness (save energy)
antidepressant drugs
- block transporter proteins that reabsorb serotonin, dopamine , norepinephrine into presyn neuron after released (block reuptake)
- NTs present in synaptic cleft for longer continue stimulating postsyn cell
increase BDNF levels over course of weeks
