RECENT reports have shown that typical neuroleptics may enhance glutamatergic neurotransmission and that these effects might in part underlie motor side effects of chronic neuroleptic treatment. Since glutamate reuptake is the primary mechanism for controlling extracellular glutamate levels, the present study was conducted to examine whether chronic neuroleptic exposure alters gene expression for the glutamate transporter GLT-1 in the striatum. Although both haloperidol and clozapine treatment for 30 days significantly decreased GLT-1 expression from normal, the effects of haloperidol treatment were consistently, and in the dorsal striatum, significantly greater than those of clozapine. These findings suggest that a deficiency in glutamate transport may underlie the pathogenesis of neuroleptic-induced movement disorders.