1998; Basavarajappa and Hungund, 1999b), and levels of AEA and 2-AG were enhanced in cultured cells treated chronically with ethanol presumably due to activation of PLA2 (Basavarajappa and Hungund, 1999a; Basavarajappa et al., 2000). Around this time, studies from other labs regarding the effects of CB1 agonists (Gallate et al., 1999) and antagonists (Arnone et al., 1997; Colombo et al., 1998; Gallate and McGregor, 1999; Rodríguez de Fonseca et al., 1999) on ethanol consumption were concluding that modulation of this receptor could significantly alter ethanol consumption. Following on these investigations and armed with a greater understanding of the biochemistry and physiology of the EC system, a plethora of studies conducted within the past decade has firmly established a role for the EC system in mediating the reinforcing properties of ethanol and the pathology of alcohol dependence. The remainder of this review will focus on recent literature examining the effects of ethanol on the EC system and the role the EC system plays in reward, ethanol consumption, and relapse.
