Ethanol has also been shown to effect glutamatergic signaling in the CeA. Roberto and colleagues [55] demonstrated that EtOH application decreases compound EPSPs and EPSCs in rat CeA neurons. Further investigation revealed that 44mM EtOH decreases both non-NMDA and NMDA R-mediated EPSPs and EPSCs by ~20%. Interestingly, EtOH inhibition of NMDA currents was significantly increased in slices obtained from animals exposed to chronic ethanol vapor; the authors suggest that these findings indicate sensitization of CeA NMDARs following chronic EtOH treatment. However, the authors do not report any signs of postsynaptic neuronal hyperexcitability in CeA slices obtained from EtOH-exposed animals. Similarly, there is no difference in paired-pulse ratios in slices from EtOH-exposed vs. naïve animals. EtOH application did significantly decrease PPF of NMDAR-mediated EPSPs and EPSCs in slices from EtOH-exposed rats (no change was observed in naïve slices).
