Stress Flashcards
stress
disturbance of homeostasis
systemic stressor
pose direct threat to survival
processive stressor
psychological, no direct threat
- asssociated w/ threats based on experience
__________ is the hub for two overlapping but distinct endocrine systems in stress response
adrenal gland
2 systems for stress response
HPA axis and adrenomedullary response
adrenomedullary response
immediate, non-specific
- fight or flight Cannon coined it
- catecholamines epinephrine and norepinephrine
HPA axis
- stressor causes CRH release from hypothalamus
- CRH travels to pituitary to release ACTH
- ACTH travels through bloodstream to adrenal cortex, targets zona fasciculata to stimulate release of GC’s like cortisol
- GC’s have many effects and targets
Selye’s main findings
- stress response is universal (same response regardless of type of stressor, and the same across species)
- chronic stress leads to illness
homeostatic concept cannot explain
anticipatory responses
allostasis
changing set point for homeostasis, allows us to function within changing conditions
- set points and responses to set points can change
example of acute vs chronic stress side effects that are related
acute: increased heart rate
chronic: hypertension
chronic stress on brain
affects hippocampus, amygdala, PFC, (etc)
- increase in neuroinflammation, decrease in neurogenesis
acute stress on brain
increase brain functioning, increase hippocampal neurogenesis (in rats), enhance memory 2 weeks after stress (integration of new hippocampal neurons into circuits)
does stress only affect hormones
no, also nervous and immune systems
basal GCs
steroid hormone released from adrenal cortex
- almost all vertebrate cells have receptors for them
- primary in humans is cortisol
cortisol
follows daily (diurnal) cycle
- highest right before wake, lowest during day (for us, opposite for mice bc they’re nocturnal)
- increases in response to stress and low blood glucose
- rhythm in adrenal gland is driven by ACTH release, which follows same rhythm
Addison’s disease
decrease in cortisol and aldosterone
- damage/dysfunction of adrenal cortex
- weight loss, nausea, etc
- low levels of salt and glucose in blood
- treatment = cortisol agonist like prednisone, increase salt diet if aldosterone levels are low
- higher does in times of illness, injury, or stress
Cushing’s disease
increased cortisol levels, increase in blood glucose levels
- weight gain, abdominal obesity, etc.
- treatment depends on cause, poss lower GC medication, surgery for tumours, etc
dexamethasone is a cortisol
agonist
GC in response to stress
takes longer to release, takes longer to affect targets
- early stress responses not bc of GC’s
Munck’s hypothesis
cortisol at low doses (daily basal levels) is permissive, at high doses is suppressive
- same hormone can have different effects based on dose
steps after a stressor
- catecholamines - immediate increase in respiration and cardiovascular rates
- immediate release of glucose and oxygen into blood
- epinephrine - delivery of oxygen to tissues
- glucocorticoids replenish energy reserves
- endorphins stop pain responses
Type 1
Mineralcorticoid receptors
- high affinity for cortisol
- basal, non-stress
Type 2
Glucocorticoid receptors
- low affinity, active when cortisol levels are high, during stress
permissive
basal levels of GCs enhance the actions of the first wave of stress-response hormones
- lack of GC’s sometime before stressor reduces a physiological resposne
stimulatory
stress-induced GC levels enhance the actions of the first wave of stress-response hormones
- elimination of stress-induced GC levels decreases physiological response to stressor
suppressive
stress-induced GC levels inhibit the actions of the first wave of stress-responseive hormones
- eliminations of stress-induced GC increases stress response
mother rat stress and son testosterone peak
shifter (to earlier), lead to impaired secual behaviour
increase LG =
increase in serotonin tone in hippocampus, increase in transcription factor NGFI-A
demethylation of GR exon 1, acetylation of histones around GR in hippocampus -> better gene expression, more GR in hippocampus, regulate stress response
low LG =
methylation at exon 17 gene region of GR gene, NFGI-A couldn’t bind as well = lower GR in hippocampi, worse stress response regulation
bullied twin =
increased DNA methylation at CpG8 on SERT = decreased cortisol response
