For many years, both ethanol and cannabinoid drugs were thought to exert the majority of their psychotropic effects through non-specific disruption of membrane lipids or alterations in the content of membrane lipids (Bruggemann and Melchior, 1983; Chin and Goldstein, 1981; Hillard et al., 1985; Hillard et al., 1990; Sun and Sun, 1985). Although there is currently not a specific receptor associated with the mechanism of action for ethanol, a robust data set has emerged in the past 20 years that strongly indicates the majority of ethanol’s actions at intoxicating concentrations are mediated by relatively weak interactions with a wide variety of molecular targets that include membrane receptors and enzymes. It is beyond the scope of this review to exhaustively describe the molecular mechanisms by which ethanol alters central nervous system (CNS) physiology (for review see Harris et al., 2008).
