Effect of Acamprosate on Glutamate Level of Alcoholic Subjects

Reza Momenan¹, John Umhau¹, Yan Zhang², Daniel Hommer¹, Markus Heilig¹, Jun Shen²

Increased alcohol preference have been related, in rodents, to repeated cycles of intoxication and withdrawal. High EtOH preference is suggested to cause a hyperglutamatergic state, which persists beyond acute withdrawal. In alcoholics, such a hyperglutamatergic state might link the acute symptoms of individual withdrawal, which may increase craving and potential for relapse. Therefore, we have hypothesized that by reducing the glutamate level we may reduce the withdrawal symptoms and hence increasing the success of abstinence. Acamprosate both reduces ethanol consumption in alcoholics and purportedly modulates glutamatergic signaling. We present results from an ongoing investigation of this effect on human alcoholic subjects.