with 1mM ethanol diminished this current following application of 30mM ethanol [30]. The efficacy of low ethanol concentrations in modulation of GABA-gated current in the CA1 hippocampal region may therefore be influenced by previous ethanol exposure. Other studies suggest that there may be pivotal developmental differences that account for differential effects of low ethanol concentrations in adolescent (P30–40) versus adult (P70–80) hippocampal neurons. Previous work demonstrates that acute ethanol (30mM) enhances tonic inhibition mediated by GABA-A receptors in dentate granule cells more effectively in adolescent as opposed to adult rats [31]. Other studies have shown that 30mM ethanol promotes firing of hippocampal interneurons, and that this enhancement in frequency of spontaneous action potentials was lower in adolescent rats compared to adults [32]. Furthermore, the amplitude of hyperpolarization-activated cation current, Ih, was also diminished to a greater extent in adolescent than adult hippocampal interneurons [32]. Interestingly, the enhancement in spontaneous firing rates is restricted to interneurons within stratum oriens [32].
