Apart from genetically modified mouse models, other studies have also implicated GABAA receptors in ethanol dependence. For instance, pentylenetetrazole-kindled animals displayed ethanol withdrawal behavior similar to animals exposed to repeated cycles of ethanol withdrawal (Davidson et al. 1999). Moreover, animals subjected to repeated withdrawals exhibit faster pentylenetetrazole-kindled seizure activity compared to controls and animals experiencing only a single ethanol withdrawal (Ripley et al. 2002). Additionally, while lorazepam could decrease HIC severity in repeated withdrawals, this intervention led to an exacerbated final withdrawal compared to animals that did not receive lorazepam during multiple withdrawals from ethanol (Becker and Veatch 2002). These results hint that this interactive effect between benzodiazepines and ethanol may involve GABAA receptors. Studies with benzodiazepines have also implicated GABAA receptors in ethanol withdrawal-related hyper-algesic effects. Diazepam reversed ethanol withdrawal hyperalgesia, but this effect could not be reversed by flumazenil (Gatch 1999). Studies have also shown that flumazenil reduces seizure severity (Buck et al. 1991b) and reverses the anxiogenic-like effects (Moy et al. 1997) associated with ethanol withdrawal. While known as a benzodiazepine antagonist, flumazenil has also been shown
