Prolonged ethanol consumption and repeated ethanol withdrawals produce many adaptations of GABAA receptor function (Table 2). For instance, ethanol exposures result in the development of tolerance to many of the GABAergic effects of ethanol including the sedative, motor incoordinating, and acute cognitive-impairing effects of ethanol (Le et al. 1986; Silvers et al. 2003c). Withdrawal from ethanol produces marked increases in CNS excitability that form a criterion for ethanol dependence (Becker et al. 1997; Devaud et al. 1996; McCown and Breese 1990; Moy et al. 2000). Substantial evidence suggests that these behavioral and neural adaptations involve marked alterations in the pharmacological properties of GABAA receptors (Table 2).
