Amphetamine-induced dopamine release and post-synaptic specific binding in patients with mild tardive dyskinesia

Several lines of evidence suggest that changes in dopamine release and/or post-synaptic sensitivity may be involved in the pathogenesis of tardive dyskinesia (TD). Preclinically, increased D-2 receptor sensitivity and dopamine turnover are associated with D-2 receptor antagonism. Clinically, development of TD is associated with D-2 receptor antagonist administration. Eight Patients With mild evidence of TD (AIMS ratings greater than or equal to 14) and six without (AIMS = 10), underwent [C-11]raclopride PET scans. Baseline and amphetamine-induced decrements in striatal specific binding were assessed. Baseline and amphetamine-induced decrements in specific binding did not differ between patients with and without evidence of mild TD (p = .53). AIMS ratings did not significantly correlate with baseline (p = .76) or decrements in specific binding (p = .45). This study provides evidence that TD is not associated with increased amphetamine-induced presynaptic dopamine release and/or D-2 receptor binding as measured by [C-11]raclopride PET. More research is needed to unravel the neurobiology of this debilitating disorder. (C) 2002 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.