Anandamide (AEA) is an endogenous cannabinoid that binds to both central cannabinoid ( CB1 ) and peripheral cannabinoid ( CB2 ) receptors. The biological actions of AEA are terminated by cellular uptake and hydrolysis of the amide bond by the enzyme fatty acid amide hydrolase. Arachidonoyl-N,N-dimethyl amide is an analog of anandamide that exhibits weak or no binding to the human central cannabinoid ( CB1 ) receptor (Ki >1 μM). It inhibits rat glial gap junction cell-cell communication 100% at a concentration of 50 μM.
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