Stress increases glucocorticoids in the brain (cortisol in humans, corticosterone in rodents). Long exposure neurodegenerative effects: mitrochondrial dysfunction, cell atrophy & death, hyperphosphorylation of cytoskeletal Tau protein which is important for dendrite remodeling
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Replying to @preinfarction @0xc020de
I'm not sure, but I think that elevated serotonin in the paraventricular nucleus of the hypothalamus leads eventually to the production of glucocorticoids in the adrenal cortex above the adrenal glands, by the kidneys,
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Replying to @preinfarction @0xc020de
Elevated serotonin, not underproduction, seems to be the problem of mood disorders, although we're really bad at measuring it in the CNS. Acute administration of SSRIs makes it worse. After chronic administration, some compensatory mechanisms must reduce serotonin levels.
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Replying to @preinfarction @0xc020de
BDNF is a peptide hormone which acts as a growth factor for neurons. Acute administration of SSRIs like fluoxetine reduces BDNF. This https://www.ncbi.nlm.nih.gov/pubmed/16842762 is the only thing I know about how chronic SSRI administration increases BDNF transcription
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Replying to @preinfarction @0xc020de
I think plasticity can mean lots of things, from dendritic remodeling to changes in connectivity following cell death to signaling pathway stuff involving astroglial cell atrophy. It's not a uniform parameter throughout the brain like temperature in simulated annealing.
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Replying to @preinfarction @0xc020de
So I'd caution against thinking of it too highly as an important explanatory variable.
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Supposedly astrocytes synthesize BDNF, GDNF, and NGF. Maybe damage to astrocytes from cortisol is enough to explain reduction in BDNF, and then {chronic SSRI -> reduced serotonin in PVN thalamus -> reduced cortisol} is enough to restore BDNF levels.
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