Stress 1 Flashcards
When the body is challenged by almost anything that happens to us, from getting out of bed in the morning or
running up a flight of stairs or having to stand up and give a talk, the brain activates two primary types of
hormones. what are they?
adrenergic (NE, EPI) and cortisol
Which Axis is produces adrenergic hormones?
SYMPATHOADRENAL AXIS
which axis produces cortisol
HYPOTHALAMIC-PITUITARY-ADRENAL AXIS (HPA)
Is the limbic system involved in stress?
yes, it regulates HPA axis via PVN of hypothalamus
SYMPATHOADRENAL AXIS generates a short or long latency?
short
SYMPATHOADRENAL AXIS is involved in the initial or latter part of the stress response?
initial
In the SYMPATHOADRENAL AXIS the Limbic system (PFC, amygdala, hippocampus) interprets threatening or intense environmental stimuli as stressful and projects this to what?
BNST!!! (bed nucleus of striaterminalis) - located just above the preopticnucleus of hypothalamus
The BNST mediate threatening info from ______ to ______ (two brain structures)
amygdala; hypothalamus
What two structures modulate reposes to threat?
PFC and hippocampus
BNST regulates ____ directly or via ______
LC; PVN of hypothalamus
what is the the largest NE pathway?
LOCUS COERULEUS (LC),
LOCUS COERULEUS (LC), the largest NE pathway, generates peripheral & central stress responses by projecting caudally or rostrally?
Both caudally and rostrally
Peripheral responses to acute stress involve which pathway?
sympathoadrenal axis
PERIPHERAL RESPONSE TO ACUTE STRESS includes Systemic responses due to endocrines (EPI & NE) released from what organ?
adrenal medulla
what two major systemic reposes occur in acute stress as a result of EPI and NE?
- Increase muscle metabolism
* Epinephrine facilitates glucagon in releasing glucose from the liver
rostral projection of LC go where to provide feedback resetting control of ANS?
PFC, hippocampus, amygdala
central responses to acute stress are determines by the type of ___ receptor activates by the ___
NE; LC
In non-stress situation, LC produces _______ levels of NE that engage high-affinity ___receptors in PFC, hippocampus and amygdala
moderate; α2
What does NE on α2 receptors receptors do?
strengthens PFC functions (attentionalselectivity) and weakens those of the amygdala and hippocampus.
acute stress leads to increased or decreased LC activity?
increased
In acute stress, high levels of NE engage lower affinity_______, which weaken ___ but strengthen _______ and _______function.
βreceptors; PFC; amygdala; hippocampal
Higher NE levels shift PFC from working memory and attentional selectivity to what?
more arousal, scanning of the environment and decision making (PFC)
Higher levels of NE shift the hippocampus and amygdala to what?
enhanced memory consolidation and fear conditioning
The HPA produces short or long term stress reposes?
both short and long!
The HPA’s responds to stress using what?
cortisol!
What is CRH
corticotrophin releasing hormone/factor
What structure is CRH released from?
PVN (paraventricular hypothalamic nucleus)
CRH transport down what to the anterior pituitary?
portal vessel
CRH transports down the portal vessel to what structure?
anterior pituitary
CRH stimulates the release of what two things from anterior pituitary cells?
ACTH and beta-endorphin
What is core leased with CRH from the PVN?
Vasopressin (VP)
What strengthens CRH’s ability to trigger release of ACTH from anterior pituitary?
VP!
VP is up-regulated or down-regulated with chronic stress?
up-regulated
What does ACTH (adrenocorticotropic hormone) do?
triggers release of glucocorticoids from adrenal cortex
what is cortisol?
human glucocorticoid stress hormone
what is cortisol derived from?
cholesterol
long term ACTH stimulation can have what effect on the adrenal cortex?
Causes upregulation, hyperplasia, and hypertrophy of the gland to produce more cortisol.
In general, what does cortisol do for you?
It prepares your limbic system for stressful situations and helps your body
maintain metabolic energy
Why does cortisol need to be restricted to times of need?
because excess cortisol can lead to tissue destruction
cortisol binds to what two corticoid receptors?
MR (mineralocorticoid) and GR (glucocorticoid)
What is cortisol’s permissive action?
at initially low levels, cortisol amplifies NE-glucagon pathway via MR to increase glucose levels
What is cortisol’s suppressive action?
Later, at high levels (via GR), cortisol is suppressive
metabolic actions: cortisol converts protons and lipids in glucose via what three biochemical processes?
- Gluconeogenesis in liver
- Proteolysis in muscle, lymphoid, skin & CT
- Lipolysis of adipose
Excess cortisol causes:
•High blood sugar
•Insulin resistance in fat & muscle (→NIDDM)
•Protein loss; wasting of muscle, bone matrix, & lymphoid tissues.
•Fat accumulation in
Abdomen (visceral and upper body fat)
Base of the neck (buffalo hump)
Face (moon face)
longterm stress resets what levels?
homeostatic levels of cortisol and its action?
Immune actions of cortisol: low cortisol has a permissive or inhibitory affect on inflammation and immunity?
permissive
How do higher levels of cortisol limit inflammation?
By reducing release of histamine, bradykinin, PGE & leukotrienes to reduce swelling, vasodilation & phagocytosis
How does high cortisol limit immunity?
By reducing cytokine release, antibody formation, cellular immunity and fever
What three structures regulate the PVN?
PFC, hippocampus, and amygdala
PFC, hippocampus, and amygdala regulate PVN via what?
BNST
CRH does other things in addition to ACTH release. In the prefrontal cortex, stress activates CRH neurons for:
Anticipation and cognition:
•mPFCreceives cognitive and emotionally salient information related to the stressor from hippocampus & amygdala, eg. memories related to past stress experiences
•CRH acting in the mPFCexerts an excitatory influence on HPA responses to acute and repeated stress via the amygdala
CRH does other things in addition to ACTH release. In the amygdala and BNST, stress activates CRH neurons for:
emotional aspects of responses (fear and anxiety) and memory
CRH does other things in addition to ACTH release. In the hypothalamus, stress activates CRH neurons for
descending pain control plus motivation and drive
CRH does other things in addition to ACTH release. In the PAG, rap he nucleus, and LC stress activates CRH neurons
to mediate the behavioral, adrenergic and serotonergic components of the stress response.
Physiological stressors representing homeostatic challenges, conveyed by sensory pathways, generate reactivestress responses through the what structure(s)?
The hypothalamus and pituitary, NOT the limbic system.
Eg. changes in cardiovascular tone, respiratory distress, visceral or somatic pain, and factors in inflammation/infection
which axis alters cognitive and emotional precesses relevant for behavioral adaptation?
HPA
Anticipatory HPA réponses are generated by what?
Limbic dependent conditioning (memory) or by innate predispositions (e.g.. recognition of danger of heights, predators). AKA they occur in absence of physiological challenges.
In anticipatory reactions, what riggers the release of cortisol?
Hypothalamic activation. This release of cortisol acts on target organs and also feeds back onto HPA and limbic structures
What is cortisol feedback important for?
It is essential to limit the duration of cortisol secretion and for prevention of deleterious effects of persistently elevated levels of cortisol on cardiovascular, immune, metabolic, and neural systems.
Normal levels of cortisol will simply inhibit HPA activity. What will persistent high levels of cortisol do instead?
Alter the functions of the limbic and HPA structures.
What structures in the HPA does cortisol feed back on?
PVN, pituitary, hippocampus, amygdala, and mPFC
Is cortisol feedback on the hypothalamus and pituitary rapid or slow? What does it consist of?
Rapid feedback: Cortisol binding to GR in PVN & pituitary cells inhibits ACTH & cortisol release following a bout of acute stress
Cortisol resistance is due to the down regulation of what kind of receptor?
GR receptors
The decrease in GR receptors seen in cortisol resistance leads to a decrease or increase in negative feedback?
decrease
The decrease of the negative feedback seen in cortisol resistance leads to an increased or decrease in ACTH & cortisol production?
increase
Hpercortisolism in seen in people with what three conditions?
chronic pain, depression, and anorexia
Supersensitivity or GR (unclear cause) _______ cortisol feedback, ______ HPA activity.
enhancing; inhibiting
What trigger hypocortisolism?
super sensitivity of GR
Where is hypocortisolism seen?
PTSD, Chronic fatigue syndrome, fibromyalgia
