Fig. 5
From: Lower circulating endocannabinoid levels in children with autism spectrum disorder
Schematic diagram of the endocannabinoid system, relevant to this study. Legend: biosynthesis, degradation, and receptors’ binding of AEA, 2-AG, OEA, and PEA are presented. AEA, PEA, and OEA are synthesized from the membrane’s phospholipids by N-acylphosphatidylethanolamine-specific phospholipase D (NAPE-PLD). PEA and OEA do not bind CB1R, but they can enhance AEA activity at transient receptor potential channels of vanilloid type-1 (TRPV1). AEA, PEA, and OEA are all degraded by fatty acid amide hydrolase (FAAH) and hence OEA and PEA can increase AEA levels by competing with AEA for FAAH (mainly OEA) or by downregulating FAAH expression (mainly PEA). Cannabidiol (CBD), a non-psychoactive component of the cannabis plant, activates peroxisome proliferator-activated receptors (PPARs) and TPRV1 and inhibits FAAH and hence might compensate for lower levels of AEA, OEA, and PEA in children with ASD. DAGL, diacylglycerol lipase; MAGL, monoacylglycerol lipase. EMT, endocannabinoid membrane transporter; GPR55, G protein-coupled receptor 55