In contrast, Melis et al. (2002) reported that a single EtOH exposure in vivo induces a long-lasting facilitation of GABA transmission in the VTA of EtOH-preferring C57BL/6 mice. These investigators observed that evoked GABAA IPSCs in dopaminergic neurons of EtOH-treated animals exhibited paired-pulse depression (PPD) compared with saline-treated animals, which exhibited PPF (Melis et al. 2002). An increase in frequency of mIPSCs was also observed in the EtOH-treated animals. Moreover, the GABAB receptor antagonist, CGP35348, shifted PPD to PPF, indicating that presynaptic GABAB receptor activation, likely attributable to GABA spillover, might play a role in mediating PPD in the EtOH-treated mice (see later GABAB paragraph). In a more recent study, the same group (Wanat et al. 2009) demonstrated that EtOH exposure also increased GABA release onto VTA dopamine neurons in EtOH non-preferring DBA/2 mice. However, a single EtOH exposure reduced glutamatergic transmission and LTP in VTA dopamine neurons from the EtOH non-preferring DBA strain but not EtOH-preferring C57BL/6 mice (Wanat et al. 2009).
