and this reduced neuroactive steroid response directly mirrors the reduced cognitive and neurophysiological effect following ethanol challenge. Therefore, it is likely that the prolonged cognitive and neurophysiological tolerance found following chronic ethanol exposure during adolescence is due to GABAergic mechanisms such as altered neuroactive steroid levels. Chronic ethanol exposure has also altered other ethanol-related behaviors in adolescents. Although sensitivity to the motor-impairing effects of ethanol increases during development, repeated adolescent binge drinking episodes prevent the emergence of this normal developmental change (White et al. 2002b). Additional studies have also revealed a persistent tolerance to the sedative effects of ethanol, resulting in continued attenuation of the animal’s loss of righting reflex (Silveri and Spear 1998; Silvers et al. 2003b).
