mM acute ethanol decreased spike frequency and input resistance supporting the idea of an inhibitory action of acute alcohol on excitability via a chloride channel [40]. Other studies have also investigated ethanol modulation of glutamatergic responses. It has been shown that concentrations of 5–10 mM ethanol inhibits NMDA-receptor mediated EPSCs in slices from the posterior cingulate cortex of rats [41]. This inhibition was more potent in cells from juveniles (PD28–32) than from adults (PD95–135). In slices from the primary somatosensory cortex of rats, concentrations of ethanol from 10–20 mM were found to have both potentiating and attenuating modulatory effects on AMPA-induced currents [42]. The outcome of ethanol modulation appeared to be age-dependent: a higher incidence of ethanol-induced potentiation was observed in neurons from rat pups of the PD6 to PD9 age group, while ethanol-induced attenuation was more prevalent in neurons from rat pups of the PD13 to PD15 age group. Other work in rat somatosensory cortical neurons has focused on the effects of ethanol on synaptically evoked responses and membrane properties. The primary effect of ethanol (10 mM) in slices from this region was to reduce neuronal excitability, measured as an increase in rheobase and a decrease in input resistance,
