ABSTRACT
Over the last century, many advances have been made in elucidating the physiological mechanisms underlying the behavioral and cognitive effects of alcohol (ethanol). Early theories suggested that ethanol partitioned into neuronal membranes in a rather nonspecific manner, thereby causing a generalized disruption of central nervous system (CNS) function (Seeman, 1974; Goldstein, 1986). Over the past 30 years, it has become increasingly clear that ethanol perturbs neuronal function in a far more
selective manner than originally thought. It is now widely appreciated that acute exposure to alcohol directly alters the activity of some of the ligand-gated ion channels that mediate excitatory and inhibitory synaptic transmission (Faingold et al., 1998; Tsai and Coyle, 1998). Alcohol also disrupts the function of a select group of voltage-gated ion channels that regulate neurotransmitter release and neuronal firing (Brodie and Appel, 1998; Dopico et al, 1999; Walter and Messing, 1999). Moreover, these same synaptic proteins appear to undergo extensive neuroadaptive changes in response to chronic alcohol exposure and withdrawal.
