There is some evidence that low doses of ethanol (EtOH) decrease excitability in the central amygdala (CeA) in rats. Roberto and colleagues [51, 52] found that 5 and 11mM EtOH increase evoked IPSC amplitude in CeA neurons. This group later found that this potentiating effect of EtOH may be mediated by CRF1 receptors, as the increased IPSC amplitude observed in CeA neurons in response to 11mM EtOH is absent in CRF1 knockout mice and blocked by a CRF1 antagonist [53]. Conversely, this group has not demonstrated an effect of low EtOH concentrations on the amplitude of spontaneous IPSCs, nor found evidence that low EtOH concentrations induce paired-pulse facilitation of CeA IPSCs [51–54]. However, they have presented evidence that acute EtOH decreases glutamatergic signaling in the CeA. Specifically, 14mM EtOH was shown to decrease compound EPSPs and EPSCs in this region [55].
