Endocannabinoids are believed to be formed in post-synaptic cells by excitatory activity and are released into the synapse where they act in a retrograde manner to activate their presynaptically located receptor and inhibit neurotransmitter release (Ohno-Shosaku et al., 2001; Schlicker and Kathmann, 2001; Wilson et al., 2001). Termination of endocannabinoid signaling is determined by metabolic enzymes. Fatty acid amide hydrolase (FAAH) is the primary catabolic enzyme of AEA, and hydrolyzes AEA into ethanolamine and arachidonic acid (Deutsch et al., 2002; Ueda, 2002). 2-AG is primarily metabolized by monoacylglyceride lipase (MAG lipase) to form glycerol and arachidonic acid (Deutsch et al., 2002; Dinh et al., 2002; Ueda, 2002).
