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Fig. 7 | The Journal of Headache and Pain

Fig. 7

From: Potentiation of endocannabinoids and other lipid amides prevents hyperalgesia and inflammation in a pre-clinical model of migraine

Fig. 7

Substrates and products of FAAH with their putative biological functions. The substrates of FAAH enzyme are bioactive amides like AEA, PEA and OEA; for example, AEA is hydrolyzed by FAAH into AA and EA. Inhibition of FAAH leads to an increase of these amides, whose function is to promote anti-nociceptive and anti-inflammatory effects through the activation of CB1/2, PPARs and GPCRs receptors. It must be however noted that, in certain circumstances, AEA can also act on TRPV1 channels causing pro-nociceptive effects. In addition, a small amount of AEA may be metabolized also by COX-2, leading to an increase in pro-inflammatory prostaglandins. For a more comprehensive and detailed description of the endocannabinoids and related lipids metabolism and biological functions, refer to [31, 32, 36]. AA = arachidonic acid; AEA = anandamide; CB1/2 = cannabinoid receptors 1 and 2; COX-2 = cyclooxygenase-2; EA = ethanolamine; FAAH = fatty acid amide hydrolase; Gly = glycerol; GPCRs = G-protein-coupled receptors; OA = oleic acid; OEA = oleoylethanolamide; PA = palmitic acid; PEA = palmitoylethanolamide; PG = prostaglandin; PPARs = peroxisome proliferator-activated receptors; TRPV1 = transient receptor potential cation channel subfamily V member 1

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