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N-arachidonoyl-serotonin inhibits FAAH and binds to the TRPV1 receptor, but has it been shown to have any activity regarding its 5-HT moiety at classical serotonin receptors?
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I suppose what I am trying to get at is; if there is an endogenous antagonist or reverse agonist produced during certain events, wouldn't this cause a rise in eCB levels (i.e. anandamide), leaving...
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