Augmentation of excitatory neuronal activity by enkephalins may be achieved by depression of firing of inhibitory γ-aminobutyric acid-ergic (GABAergic) neurons (1–3). The latter findings and consideration of roles of GABAergic neurons in information processing in the central nervous system (4–7) led one of us (E.R.) to propose that the effects of low doses of naloxone be investigated in disorders in which there may be excessive disinhibition, among which may be tardive dyskinesia (TD). We now report results obtained with two schizophrenic women with TD who were given naloxone in a short-term, double-blind study.