Arachidonoyl serotonin (N-arachidonoyl-serotonin, AA-5-HT) is an endogenous lipid signaling molecule. It was first described in 1998 as being an inhibitor of fatty acid amide hydrolase (FAAH).[1] In 2007, it was shown to have analgesic properties and to act as an antagonist of the TRPV1 receptor.[2] In 2011, it was shown to be present in the ileum and jejunum of the gastrointestinal tract and modulate glucagon-like peptide-1 (GLP-1) secretion.[3] In addition to this, in 2016, AA-5-HT was also found to affect the signaling mechanisms responsible for anxiety, by inhibiting dopamine release from the Basolateral amygdala following fear behavior.[4] In 2017, AA-5-HT was tested in its effects on the sleep wake cycle, where it was found to affect the sleep homeostasis when used in conjunction with molecules and chemicals that affect wake-related neurotransmitters.[5]
^ Bisogno, T.; Melck, D.; De Petrocellis, L.; Bobrov, M. U.; Gretskaya, N. M.; Bezuglov, V. V.; Sitachitta, N.; Gerwick, W. H.; Di Marzo, V. (1998). "Arachidonoylserotonin and other novel inhibitors of fatty acid amide hydrolase". Biochemical and Biophysical Research Communications. 248 (3): 515–522. doi:10.1006/bbrc.1998.8874. PMID9703957.
^ Verhoeckx, K. C. M.; Voortman, T.; Balvers, M. G. J.; Hendriks, H. F. J.; m.Wortelboer, H.; Witkamp, R. F. (2011). "Presence, formation and putative biological activities of N-acyl serotonins, a novel class of fatty-acid derived mediators, in the intestinal tract". Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. 1811 (10): 578–586. doi:10.1016/j.bbalip.2011.07.008. PMID21798367.
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