Role of Glutamate in Alcohol Withdrawal Kindling

Abstract

It is well known that continued excessive alcohol consumption can lead to the development of physiological dependence. When drinking is abruptly terminated or substantially reduced in the dependent individual, a characteristic withdrawal syndrome ensues. As with other central nervous system (CNS) depressants, withdrawal symptoms associated with cessation of chronic alcohol use are opposite in nature to the effects of intoxication. Thus, clinical features of alcohol withdrawal include signs of heightened autonomic nervous system activation (e.g., tachycardia, elevated blood pressure, diaphoresis, tremor), CNS hyperexcitability that may culminate in motor seizures, and, in its most severe form, hallucinosis and delerium tremens (1–3). In addition to physical signs of withdrawal, a constellation of symptoms contributing to psychological discomfort (e.g., irritability, agitation, anxiety, dysphoria) constitute a significant component of the withdrawal syndrome (4–7). The overall intensity of the withdrawal syndrome is presumed to reflect the degree of physiological dependence developed during the course of chronic alcohol use/abuse.