Subchronic continuous phencyclidine administration potentiates amphetamine-induced frontal cortex dopamine release.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology January 1, 2003 Andrea Balla, Henry Sershen, Michael Serra et al.
Dopaminergic hyperactivity in the prefrontal cortex (PFC) may contribute to cognitive dysfunction in schizophrenia. In rats, subchronic treatment with phencyclidine (PCP) at doses of 10 mg/kg/day or higher produced serum concentrations associated with PCP psychosis in humans. PCP-treated rats showed a significant, dose-dependent enhancement in amphetamine-induced dopamine release in the PFC but not in the nucleus accumbens (NAc), along with increased locomotor activity. This enhanced response appeared after 3 days of treatment, persisted through 14 days, and resolved within 4 days of withdrawal. The findings suggest that NMDA receptor dysfunction could underlie the dopaminergic abnormalities seen in schizophrenia and that even short-term PCP abuse may potentiate the effects of psychostimulants.