On the other hand, drugs with some selectivity for α4-subunits (e.g., RO 15-4513 and DMCM) showed an increased modulation of mIPSCs possibly reflecting the increase in α4 subunit expression (Kang et al. 1996, 1998a, b). Interestingly, the evoked IPSCs were still sensitive to alphaxalone (Kang et al. 1998b) suggesting differences in the populations of GABAA receptors that underlie evoked and mIPSCs. In addition, the acute effect of EtOH on evoked IPSCs was significantly increased in slices from chronic EtOH-exposed rats (Kang et al. 1998a, b). Liang et al. (2004) have also compared the effects of chronic EtOH exposure on synaptic and extra-synaptic receptor functions in CA1 neurons. These investigators found similar alterations in the synaptic mIPSCs and the tonic extrasynaptic GABAA receptor-mediated conductance associated with chronic EtOH exposure. Both mIPSCs and the tonic current show profound tolerance to α1-containing GABAA receptor selective doses of diazepam and zolpidem (Cagetti et al. 2003). As previously demonstrated (Grobin et al. 2000), chronic EtOH exposure results in a decrease in BZP-sensitive α1-subunits and an increase in BZP-insensitive α4-subunits at synaptic receptors. Thus, THIP (a
