 The purpose of this study is to investigate the interaction between glycine and D-cycloserine in alcoholic patients and healthy subjects. Preclinical studies have shown that compounds acting at the glycine site of the N-methyl-D-aspartate NMDA receptor complex, such as glycine, may reverse the effects of ethanol on the NMDA receptor function Rabe et al., 1990. The amino acid glycine is a co-agonist of the NMDA receptor complex Kemp et al., 1993. It binds to the strychnine-insensitive site and positively modulates the NMDA receptor Mc Donald et al., 1990. Physiologically, the glycine site is not saturated, and administration of glycine can potentiate NMDA receptor mediated responses. In contrast, D-cycloserine Hood et al., 1989 is a partial-agonist at the glycine site of the NMDA receptor, with dose-dependent NMDA antagonist properties. The NMDA antagonist activity of D-cycloserine should produce ethanol like-effects that can be reversed by the agonist glycine. This study is intended to evaluate possible contributions of the glycine site to the reduction of cognitive deficits of alcoholism and complements the current work at VA Connecticut Healthcare System on the NMDA antagonists in alcoholic and healthy subjects. 