The functional interactions of neuropeptides (CRF, NPY, nociceptin) with GABAergic and glutamatergic systems may play major roles in the acute effects of EtOH on GABAergic and glutamatergic transmission. Understanding the underlying mechanisms of these interactions may offer a possible avenue for restoring “normal” function following chronic drug exposure. The neuroadaptations induced by chronic EtOH on GABAergic and glutamatergic systems may represent homeostatic or compensatory mechanisms in response to the acute EtOH actions on these systems.
