The same group [53] later replicated the finding that 22 and 44 mM EtOH increase IPSC amplitude. However, EtOH had no effect on IPSC amplitude in CRF1 knockout mice. Similarly, superfusion of a CRF1 antagonist ablated the potentiating effect of 44mM EtOH on IPSC amplitude in slices obtained from wild type mice. Herman and colleagues [54] recently investigated these earlier findings more closely by making use of CRF1:GFP reporter mice. These authors found that CRF1-expressing neurons exhibit a GABAA receptor α1 subunit-mediated tonic conductance, and that EtOH (44mM) increases the firing rate of these cells. Conversely, CeA neurons that did not express CRF1 display a δ-subunit mediated tonic conductance that is enhanced by EtOH, and EtOH superfusion decreases the firing rate of these cells. Interestingly, EtOH application does not alter sIPSC frequency in the majority of CRF1+ neurons, but does increase sIPSC frequency in all CRF1- neurons. Consistent with previous reports by members of this group [51] no EtOH-induced alterations in sIPSC amplitude were observed in either cell population. Finally, retrograde tracing studies revealed that these CRF1-containing neurons project to
