2008). Mitrirattanakul et al (2007) reported that rats made ethanol dependent using a chronic intermittent ethanol regimen displayed increased levels of AEA and 2-AG in the hippocampus that persisted 40 days into withdrawal. Additionally, mice treated with ethanol vapor for 72 hrs displayed increased concentrations of AEA in cortex that were correlated with decreased activity of FAAH (Vinod et al., 2006), and similar results were obtained in cultured cerebellar neurons where enhanced media levels of AEA were associated with reduced activity of FAAH and EC transport mechanisms following chronic ethanol treatment (Basavarajappa et al., 2003). Results from a post-mortem study of human tissue also found reduced expression and activity of FAAH in the ventral striatum of alcoholic patients, and these changes in FAAH were correlated with enhanced tissue content of AEA and reduced expression of CB1 (Vinod et al., 2010). In addition to studies with ethanol, FAAH KO mice display reduced CB1 expression and G-protein coupling in several brain regions including the striatum, hippocampus, NAc, and amygdala (Vinod et al., 2008a). Together these results suggest that the increased levels of ECs following chronic ethanol may arise from enhanced synthesis and reduced inactivation mechanisms. However, to fully establish the causative role
