Acute sleep deprivation upregulates serotonin 2A receptors in the frontal cortex of mice via the immediate early gene Egr3
ncbi.nlm.nih.gov/pmc/articles/P…
Substantial upregulation of 5-HT2A after just 6–8 hrs
5-HT2A also mediate the hallucinogenic effects of psychedelic drugs
#raypeat
ncbi.nlm.nih.gov/pmc/articles/P…
Substantial upregulation of 5-HT2A after just 6–8 hrs
5-HT2A also mediate the hallucinogenic effects of psychedelic drugs
#raypeat
pubmed.ncbi.nlm.nih.gov/18771015/
Post-mortem data shows reduced EGR3 and 5-HT2A in the prefrontal cortex of schizophrenics vs. controls, implying that the upregulation is compensatory and due to low binding ability.
pubmed.ncbi.nlm.nih.gov/27179966/
Post-mortem data shows reduced EGR3 and 5-HT2A in the prefrontal cortex of schizophrenics vs. controls, implying that the upregulation is compensatory and due to low binding ability.
pubmed.ncbi.nlm.nih.gov/27179966/
The post-mortem schizophrenic patients showed 6 antibodies indicating immunoreactivity, specifically in the brain, against histone proteins.
"Each of the 6 antihistone antibodies resulted in robust immunoreactivity of nuclei in the prefrontal cortex"
"Each of the 6 antihistone antibodies resulted in robust immunoreactivity of nuclei in the prefrontal cortex"
Top-down or bottom-up, the hypometabolism in neuropsychiatric illness like schizophrenia involves ATP and GTP deficiency, disrupting gene-and-protein expression and modification, leading to molecular chaos, which then, in a vicious circle, causes maladaptive epigenetic imprinting 
A deep read of the literature can get one bogged down in theory and mechanism. We already know empirically that neuropsychiatric illness is resolvable via elimination diets, heavy metal chelation (search 'Cutler Protocol') circadian rhythm repair, orthomolecular therapy, etc.
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