D
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God make my neurotransmitters great inc
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as far as chronic LSD administration downregulating the number of 5HT2a receptor sites:
https://www.ncbi.nlm.nih.gov/pubmed/3374263 https://www.ncbi.nlm.nih.gov/pubmed/3374263
etc.
I'm finding that a number of 5HT2a antagonists paradoxically also downregulate the receptor.
https://www.ncbi.nlm.nih.gov/books/NBK1853/
Peat has said LSD in doses below 20 mcg nuke serotonin levels and also that cyproheptadine does the same, but one is agonist and other is antagonist- so the lock and key receptor model of modern psychiatry is flawed.
@pessimistic @TsarTsar444
https://www.ncbi.nlm.nih.gov/pubmed/3374263 https://www.ncbi.nlm.nih.gov/pubmed/3374263
etc.
I'm finding that a number of 5HT2a antagonists paradoxically also downregulate the receptor.
https://www.ncbi.nlm.nih.gov/books/NBK1853/
Cyproheptadine was not specifically looked at in the research that adumbrated this oddity. I would say it is not really that dissimilar in its affinities or structure from tricyclic antidepressants, but cyproheptadine also blocks the other 5HT2 receptor subtypes effectively.A striking observation that has arisen through studies on 5-HT2A receptor levels is that chronic application of agonists like DOI, 5-HT and LSD, as well as antagonists like mianserin, ketanserin, and pipamperone, cause down-regulation of the receptor. The biochemical mechanisms behind this “paradoxical regulation” of the 5-HT2A receptor are unknown. Agonist-induced long-term regulation has been examined in numerous studies
Peat has said LSD in doses below 20 mcg nuke serotonin levels and also that cyproheptadine does the same, but one is agonist and other is antagonist- so the lock and key receptor model of modern psychiatry is flawed.
@pessimistic @TsarTsar444