Physiology of stress Flashcards
physical VS psychological stressors:
- Physical stressors are stimuli that produce actual disturbances of
the physiological status, which overwhelm the organism, e.g.,
hemorrhage and infection are considered as physical stressors. - Psychological stressors are generally defined as stimuli that
threaten the current state and are perceived in an anticipatory
condition e.g., aversive environmental stimuli, predator-related
cues and failure to satisfy internal drives.
physical stress process:
- mainly processed by the brainstem and hypothalamic regions
- usually require immediate systemic reaction, which might be considered reflexive
- 1st phase of stress response: [activation of autonomic nervous system including sympathetic nervous system (SN) and sympathetic adrenomedullary system (SAM)], provides a rapid physiological adaptation, resulting in alertness, appraisal of the situation, and decision making
- 2nd phase: involves the hormonal mechanism (Hypothalamic-Pituitary-Adrenal axis—HPA) considered sluggish
compared to the first phase, resulting in an amplified and protracted secretory response.
psychological stress process:
Psychological uncontrollable and social-evaluative threatening stressors elicit both physical and cognitive stress responses.
These responses include the activation of the autonomic nervous system (SN and SAM), HPA system and several CNS
structures, including components of limbic circuits such as the PFC, amygdala, hippocampus (HIPPO), PVN, ventral tegmental area (VTA) and nucleus accumbens (NAc)
slide 12 !!
Acute stress:
The stressors producing acute stress are relatively recent and short in
duration (<2 days to 4 weeks).
The Fight-or- Flight Response is elicited.
The SN/SAM/HPA systems are activated, while the parasympathetic
nerve system is typically diminished.
Removal of the stressor should restore normal conditions rapidly. But
sometimes this is delayed
autonomic nervous system and HPA axis:
slide 14
SN and SAM axis:
- Major Response 1: Stimulation of mental
activities. - Major Response 2: Release of epinephrine from
the adrenal medulla. - Major Response 3: Cardiovascular
o Increased heart rate and strength of cardiac
muscle contraction.
o Increased volume of blood pumped by the
heart per minute (cardiac output ).
o Constriction of arterioles in many (not all)
areas of the body.
o Increased arterial blood pressure.
o Increased blood flow to active skeletal
muscles and the heart.
o Decreased blood flow to GI tract, kidneys and
other relatively inactive organs - Major Response 4: Metabolic
o Increased cellular metabolic
rates, body-wide.
o Increased blood glucose
concentration.
o Increased liver and muscle
glycolysis.
o Increased blood coagulation
rate (to minimize blood loss if
injury occurs)
adrenal cortex and medulla hormones:
(3 zones):
- zona glomerulosa:
mineralocorticoid (MC,
e.g. aldosterone)
- zona fasciculata:
glucocorticoids (GC) and
androgens
- zona reticularis
androgens and
glucocorticoids
Adrenal medulla- catecholamines
(epinephrine, norepinephrine, and
dopamine)
(slide 17)
The hypothalamic-pituitary-adrenal axis:
(CRH = Corticotropin-
Releasing Hormone:
from paraventricular
nucleus (PVN)
ACTH = Adreno-
corticotropic
Hormone)
- The major stimulating factor for ACTH is CRH, which is regulated by
incorporation of neural and other
hormonal signals in the hypothalamus. - Circulating cortisol is the major
inhibitory factor for CRH and ACTH
secretion, through regulating gene
expression
(slide 18)
Major Brain Structures Involved in Stress Responses:
- Cerebral cortex (prefrontal cortex, especially).
- Limbic system: receives a lot of sensory inputs:
Amygdala
Hippocampus
Hypothalamus: receives inputs from the prefrontal
cortex, amygdala, etc. - Brain stem
Medulla oblongata: cardiovascular and respiratory system
responses.
Locus coeruleus: norepinephrine neuronal system;
projects to other areas of the brain; increases level of
arousal of the brain.
Raphe nuclei: serotonin neuronal system; projects to
other areas of the brain.
effects on metabolism:
i.Anti-insulin effects
ii.Permissive action
for glucagon and
catecholamine
Vascular effects
Permissive action for
catecholamine: (arrow up and alpha)
receptors
Immune response
Anti-
inflammation
Stress itself can be both pro- and anti-inflammatory through SAM or HPA:
- glucocorticoids initially present anti-inflammatory action, but
later sensitize the immune response on the recovery phase. CRH
regulates the immune system.
Immune system also affects the CNS, modulating the HPA axis.
e.g. social stressors increase expression of proinflammatory
cytokines and activate microglia in PFC, amygdala and
hippocampus, whereas physical stressors promote an increase
in proinflammatory reactions in the hypothalamus.
Endorphins, elevated with stress, are immunosuppressive.
Growth hormone and prolactin, which are immunoenhancing
factors, are generally reduced under conditions of prolonged stress.
relationship stress and immune system (easily explained)
- Glucocorticoids initially reduce inflammation but later restore and sensitize the immune system for recovery.
- CRH and the HPA axis regulate both stress responses and immune function, while the immune system can, in turn, influence the brain and stress pathways.
- Different types of stressors affect brain regions differently, promoting inflammation in specific areas of the brain.
- Stress also affects immune function by raising levels of endorphins (which suppress the immune system) and lowering levels of growth hormone and prolactin (which normally enhance immune function), especially during prolonged stress.
feedback effects of cortisol on the brain:
slide 22
terminating stress responses:
- Feedback inhibition of cortisol on the release of CRH and ACTH
- Feedback influences of cortisol on the hippocampus, which then
turns off the HPA response - The neural circuit that connects the hippocampus to the PVN is
critical for the termination of the stress response - Lesions along this circuit lead to overexpression of CRH mRNA in
the PVN and long durations of the stress response. - Environmental and psychosocial factors that disrupt the
hippocampus can also lead to excessive levels of glucocorticoids,
which can in turn further damage the hippocampus.
terminating stress responses (easily explained):
Cortisol exerts feedback inhibition on CRH and ACTH release, helping to regulate the stress response.
The hippocampus plays a vital role in shutting off the HPA axis by influencing the PVN, forming a crucial neural circuit for terminating stress responses.
Damage to this circuit can lead to chronic stress responses due to excessive CRH production.
Environmental and psychosocial stressors that impair hippocampal function can result in increased glucocorticoid levels, perpetuating a cycle of stress and potential hippocampal damage.
