Long-Term Ethanol and Corticosterone Co-Exposure Sensitize the Hippocampal CA1 Region Pyramidal Cells to Insult During Ethanol Withdrawal in an NMDA GluN2B Subunit-Dependent Manner

Chronic ethanol (EtOH) exposure produces neuroadaptations in NMDA receptor function and/or abundance and alterations in hypothalamic–pituitary–adrenal (HPA) axis functioning that contribute to neuronal excitation and neurotoxicity during ethanol withdrawal (EWD). Both EtOH and corticosterone (CORT) promote synthesis of polyamines, which allosterically potentiate NMDA receptor function at the