Despite the early flurry of research concerning the interactions between marijuana and ethanol in the 1970s, there was a marked paucity of studies examining the intersection of ethanol and cannabinoid substances through the 1980’s and most of the 90’s. Although it was not realized at the time, the first reports to implicate ethanol as a modulator of EC biosynthetic enzymes demonstrated that chronic exposure to ethanol in mice up-regulated the activity of PLA2 and that this effect persisted into withdrawal (Hungund et al., 1994; John et al., 1985). Hungund’s lab followed up on these studies demonstrating the specific up-regulation of a Ca2+-dependent, arachidonic acid-specific isoform of PLA2 following chronic ethanol (Basavarajappa et al., 1997). Shortly thereafter, it was found that CB1 receptor expression and function were decreased in the brains of mice chronically exposed to ethanol vapor (Basavarajappa et al., 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
