 The chronic negative symptoms of schizophrenia remain poorly responsive to psychopharmacologic treatment. The impaired motivation of primary deficit syndrome patients prevents them from pursuing social and occupational goals and prevents them from developing meaningful and productive lives. This proposal is based on the test of a hypothesis that schizophrenic patients with enduring deficit symptoms suffer from impairments in reward processing and the translation of perceived reward salience into goal-oriented behavior. Preclinical and clinical research has revealed the functioning of a distributed neural network in the processing of reward stimuli. Regions of the prefrontal cortex PFC such as orbitofrontal cortex OFC and anterior cingulate cortex ACC are key frontal cortical elements of a neural circuit that mediates reward salience, reward expectation, and reward approach behavior. Aripiprazole, in virtue of its activity as a dopamine DA partial agonist, is uniquely suited to enhance functioning of these frontal areas crucial to reward processing. We hypothesize that primary deficit syndrome schizophrenia is associated with functional deficits in reward circuitry detectable by fMRI scanning during a monetary reward task. We further hypothesize that treatment with aripiprazole will normalize reward circuit function in these subjects and thus contribute to improvements in negative symptoms. The following specific aims will test these hypotheses: 