Recent animal experiments suggest that glutamate plays a fundamental role in the control of psychomotor activity. This is illustrated by the finding that even in the virtually complete absence of dopamine, a marked behavioral activation is produced in mice following suppression of glutamatergic neurotransmission. This article discusses the possibility that a deficient activity within the cortico-striatal glutamatergic pathway is an important pathophysiological component in some cases of schizophrenia and that glutamatergic agonists may prove beneficial in this disorder. In a broader perspective, schizophrenia may be looked upon as a syndrome induced by a neurotransmitter imbalance in a feedback-regulated system, where dopamine and glutamate play a crucial role in controlling arousal and the processing of signals from the outer world to the cerebral cortex via the thalamus.