Anandamide (AEA), an endogenous cannabinoid, interacts with both central (CB1) and peripheral (CB2) cannabinoid receptors. Its effects are concluded through the cellular uptake and enzymatic breakdown of its amide bond by fatty acid amide hydrolase. Arachidonoyl-N-methyl amide, an analog of anandamide, specifically targets the human CB1 receptor, displaying a binding affinity with a Ki of 60 nM. It completely inhibits rat glial gap junction intercellular communication at a concentration of 50 µM.