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

Caleb M. Adler, Anil K. Malhotra, Igor Elman, David Pickar, Alan Breier

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


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 D2 receptor sensitivity and dopamine turnover are associated with D2 receptor antagonism. Clinically, development of TD is associated with D2 receptor antagonist administration. Eight patients with mild evidence of TD (AIMS ratings ≥ 14) and six without (AIMS = 10), underwent [11C]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 D2 receptor binding as measured by [11C]raclopride PET. More research is needed to unravel the neurobiology of this debilitating disorder.

Original languageEnglish (US)
Pages (from-to)295-300
Number of pages6
Issue number3
StatePublished - 2002
Externally publishedYes


  • Amphetamine
  • Dopamine
  • PET
  • Raclopride
  • Striatum
  • Tardive dyskinesia

ASJC Scopus subject areas

  • Pharmacology


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