Studies in the hippocampus show that chronic EtOH exposure decreased long-term potentiation (LTP) by increasing the electrically stimulated (but not basal) release of tritiated GABA pre-loaded in CA1 hippocampal slices (Tremwel et al. 1994). The GABA uptake or GABAAR function was not altered, and this effect may be due to alterations in the muscarinic receptor regulation of GABA release at presynaptic terminals (Hu et al. 1999). In addition, studies using the GABAB receptor agonist baclofen to reduce release of tritiated GABA suggest that a change in GABAB auto-receptors on GABAergic terminals may also contribute to this effect of chronic EtOH exposure on LTP (Peris et al. 1997) (see later GABAB paragraph). For a general review of brain region specific EtOH actions on the GABA system see (Criswell and Breese 2005; Siggins et al. 2005; Weiner and Valenzuela 2006). More recent studies also reported that chronic EtOH consumption induces tolerance to the impairing effects of acute EtOH treatment on induction of LTP in rat CA1 slices (Fujii et al. 2008). In CA1 slices from control rats, stable LTP was induced by
