Healthy controls were matched for gender, age, race, and parental socioeconomic status. Patients had been off medication for

at least 21 days at the time of the study. Seven were neuroleptic naive, experiencing a first episode of the illness. Patients were recruited under two modalities. Seventeen patients were recruited shortly after admission to the hospital for clinical reasons and were experiencing an episode of clinical deterioration at the time of Inhibitors,research,lifescience,medical recruitment. In all cases, the admission was voluntary. The other 17 patients were recruited in outpatient enzyme inhibitor clinics. These patients were in a stable phase of the illness, and were admitted to the hospital only for the purpose of the study. In the control subjects, the amphetamine-induced reduction in [123I]IBZM BP was 7.5±7.1% (n=36). Compared with the controls, the patients with Inhibitors,research,lifescience,medical schizophrenia displayed a marked elevation of amphetamine-induced [123I]IBZM displacement. (17.1 ±13.2%, n=34, P=0.0003, Figure 1). A similar finding has been reported by Breier et al38 using [11C]raclopride, Inhibitors,research,lifescience,medical PET, and a smaller dose of amphetamine (0.2 mg/kg, intravenously). This increased effect, of amphetamine on [123I]IBZM BP in patients with schizophrenia was not related to differences in amphetamine plasma disposition, since amphetamine plasma levels were similar in both groups.

Providing that, the affinity of D2 receptors for DA is unchanged in this illness (see discussion in reference 46), these data are consistent with an increased Inhibitors,research,lifescience,medical amphetamine-induced DA

release in schizophrenia. figure 1. Effect of amphetamine (0.3 mg/kg) on [123I]iodobenzamide ([123I]IBZM) binding in healthy controls and untreated patients with schizophrenia. The y axis shows the percentage decrease in [123I]IBZM binding potential induced by amphetamine, which is a measure … The amphetamine effect on [123I]IBZM BP was similar in chronic/previously treated patients (16.2±13.5%, n=27) and first-episode/neuroleptic-naive patients (20.9±12.2%, n=7, P=0.41), and Inhibitors,research,lifescience,medical Anacetrapib both groups were significantly different from controls. In the previously treated group, no association was found between the duration of the neuroleptic-free period and the amphetamine-induced [123I]IBZM displacement (r=0.02, P=0.91). Together, these results indicated that the exaggerated dopaminergic response to amphetamine exposure was not a prolonged side effect of previous neuroleptic exposure. In patients with schizophrenia, the amphetamine challenge induced a significant, increase in positive symptoms. The emergence or worsening of positive symptoms was transient, and patients returned to their baseline symptomatology within a few hours of the challenge. We observed a significant correlation between the increase in positive symptoms and the [123I]FBZM displacement (r=0.54, P=0.0009).