Another study assessed the impact of EtOH on postsynaptic GABAB receptors via baclofen-induced hyperpolarization of hippocampal CA1 and CA3 pyramidal neurons. These receptors activate outward K+ currents via a pertussis toxin-sensitive G protein cascade to reduce membrane potential during the slow inhibitory postsynaptic potential and may play a role in EtOH intoxication and withdrawal excitability. In both types of pyramidal neurons, baclofen applied consecutively in increasing concentrations caused concentration-dependent hyperpolarization. There were no significant differences in resting membrane potential, input resistance, maximum baclofen-induced hyperpolarization, or EC50 between CA1 and CA3 neurons, although slope values were significantly smaller in the former neurons. These parameters were not significantly changed in the presence of EtOH 10–100 mM. Chronic EtOH treatment (12 days) did not shift sensitivity or maximum response to baclofen in CA1 neurons. These results suggest that GABAB receptors in this model were essentially insensitive to EtOH (Frye and Fincher 1996).
