Part 2 Flashcards
What are the three stages of stress according to Hans Selye?
Alarm stage (HPA, sympathetic activation, fight/flight) Resistance stage (physiological arousal set point is higher) Exhaustion stage (increased disease susceptibility)
What are the two primary hormones involved in the stress response?
adrenaline(NE/EPI) and cortisol
What does the adrenergic stress response system do?
sympathetic nervous system/adrenal medulla affects physiological alertness, increasing HR, BP, activates cerebral cortex, scans the environment
What does the cortisol stress response system do?
the HPA axis
enhances emotional arousal
promotes motivational, cognitive processes, aids memory, facilitates immune system readiness but can lead to allergy/autoimmune disorders is persistent
(permissive/suppressive effects)
how does the limbic system regulate the HPA axis?
via the PVN of the hypothalamus
What parts of the limbic system are involved in the stress response?
amygdala, hippocampus, limbic cortex
What is the pathway from external stimuli to the hypothalamus?
stimulus –>limbic system –>BNST which modulates amygdala–>hypothalamus
How does the BNST regulate the limbic cortex?
directly and via the PVN of the hypothalamus
cue threat processing is mediated by the ______, but sustained anxiety is mediated by _______ and ______.
cue threat –>amygdala
sustained –> tonic BNST engagement and ventral basal forebrain structure
The locus coeruleus projects NE caudally in order to _____ and rostrally in order to ______
caudal: activate sympathetic response, cause release of NE from adrenal medulla
rostral: neurofeedback to PFC, hippocampus and anygdala, to help reset limbic ANS controls
What are three responses to EPI and NE in the acute stress response?
increased muscle metabolism, EPI facilitates glucagon in releasing glucose from the liver, symp innervation of the heart, lungs, vessels and viscera
in non-stressed situations, moderate levels of NE engage ______receptors, strengthening _______functions and weakening responses from the ________ and ____________
in non-stressed situations, moderate levels of NE engage a2 receptors, strengthening PFC functions and weakening responses from the amygdala and hippocampus
in stressed situations, high levels of NE engage ______ receptors, weakening _____________functions and strengthening ________ and ____________ functions.
in stressed situations, high levels of NE engage B receptors, weakening PFC functions and strengthening amygdala and hippocampus functions.
high levels of NE cause what kinds of shifts in function of the PFC, amygdala and the hippocampus
PFC functions less in working memory, more in scanning, arousal and decision making
H and A enhance fear conditioning and memory consolidation
What is the pathway of the HPA axis?
hypothalamus releases corticotropin releasing hormone from the PVN.
CRH goes to the anterior pituitary, –> ACTH and B-endorphin released from the anterior pituitary.
–>adrenal gland
CRH release patterns are partly determined by ___________
early life events
Vasopressin is released from the _______ and does ______
released from the PVN and potentiates the ability of CRH to trigger ACTH release. (this effect is upregulated during chronic stress)
ACTH is derived from______ and triggers release of _______from _______
ACTH is derived from pro-opiomelanocortin protein and triggers the release of glucocorticoids from the adrenal cortex
Long term ACTH stimulation can cause ______ and ______ of the adrenal gland
hypertrophy and hyperplasia
cortisol binds to high affinity ______ and low affinity _____receptors
high affinity mineralocorticoid and low affinity glococorticoid receptors
The permissive actions of cortisol occur at ______ (low/high) levels of cortisol and bind _____receptors, causing an _________(inc/dec) in glucose levels
The permissive actions of cortisol occur at low levels or cortisol and bind MR receptors, causing an increase (inc/dec) in glucose levels
The suppressive actions of cortisol occur at __________(low/high) levels of cortisol and function through the binding of ________receptors
occur at high cortisol levels via binding of the GR receptor
Is cortisol anabolic or catabolic?
catabolic
What are three metabolic functions of cortisol at low levels?
gluconeogeneis, proteolysis, lipolysis
What are four metabolic effects of excess cortisol?
high blood sugar, insulin resistance, protein loss (muscle wasting), fat accumulation
What are two immune effects of excess cortisol?
inhibition of inflammation and immune response (impaired reactions to trauma or foreign substances)
What type of immune reaction does the body have to low levels of cortisol?
permissive effect on inflammation and immunity
What areas of the cortex regulate the hypothalamus? What type of regulation is it? (inhibitory/excitatory)?
PFC, hippocampus, amygdala regulate the PVN (via the BNST). largely inhibitory (GABA), but certain PFC areas can enhance HPA activity
stress activates CRH neurons in the PFC for:
aniticpation/cognition (mPFC specifically, recieves salient information related to the stressor from the hippocampus, amygdala eg. memories of past experience)
CRH acting on the mPFC causes:
excitatory influence on the HPA axis
stress activates CRH neurons in the amygdala and BNST for:
emotional aspects of responses and memory
stress activates CRH neurons in the hypothalamus for:
descending pain control plus motivation and drive
stress activates CRH neurons in the PAG, raphe nucleus and locus coeruleus to:
mediate behavioral, adrenergic and serotonergic components of stress response
What are some reactive responses to stress and what system regulates this?
changes in cardivascular tone, respiratory distress, visceral/somatic pain, inflammation, infection
mediated by the HPA axis
What is an anticipatory reaction? what is it dependent on?
a physiological reaction that occurs in the absence of a physiological stimuli. functions via the HPA axis, but dependent on limbic conditioning (motivational loop)
What causes the termination of HPA axis activation?
cortisol feedback (but changes to limbic (psychogenic) and BNST (systemic) during chronic stress causes chronic stress states)
Cortisol binds to GR receptors in the _______ and ______ to inhibit ACTH and cortisol release following a bout of acute stress (rapid cortisol feedback)
in the PVN and pituitary
How does cortisol resistance occur?
increased chronic levels of cortisol cause a decreased number of GR receptors to be expressed, leading to decreased cortisol feedback to the PVN and pituitary
What is hypercortisolism and what conditions is it seen in (3)?
increased ACTH and cortisol production after GR downregulation and cortisol resistance. occurs in: chronic pain, depression, anorexia
What is hypocortisolism and what conditions is it seen in (3)?
supersensitivity of GR that enhances cortisol feedback and decreased the amount of cortisol. occurs in: PTSD, chronic fatigue syndrome, fibromyalgia
What type of receptors are MR and GR receptors?
ligand-driven transcription factors that bind DNA directly
In the kidney, MR binds mainly _______. In the brain MR only binds _______.
aldosterone, cortisol
What is the fast response to cortisol?
cortisol binds MR first, increasing excitability of the hippocampus to sensory information. this maintains the basal activity of the HPA axis
What is the slow response to cortisol?
as cortisol rises, it binds GR. GR activity leads to inhibition of the stress response (feedback) (unless chronic)
When in the stress response does memory formation occur?
the third phase (recovery/adaptation), when cortisol binds GR
How can cortisol facilitate learning?
stress within the learning context leads to release of NA, CRH and CORT, which facilitate perception and attention. thus consolidation of learning can occur while the input of unrelated information is inhibited
How can cortisol impair learning?
If stress precedes learning, gene-mediated suppression of activity impair learning
Does cortisol inhibit or help in memory recall?
inhibits recall
How does cortisol feedback affect the amygdala?
in increases the amygdalas response to NE, producing stress related fight/flight/risk assessment behavior and learning
How does cortisol affect the PFC during acute stress?
cortisol activates the mPFC to improve working memory and terminate HPA stress responses
How does cortisol affect the PFC during greater stress?
working memory is disrupted creating distractability
How does cortisol affect the PFC during chronic stress?
GR downregulated, impaired negative feedback, enhanced HPA activity (hypercortisolism)
What is an effect of excess cortisol on top-down/bottom-up regulation of the amygdala?
reduced top-down regulation of the amygdala by the PFC
What is the extrahypothalamic CRF stress system?
cortisol actually increases synthesis of CRF in the BNST and the amygdala, providing means to extend the stress response to allostasis
