Abstract
Tardive dyskinesia may result from neuroleptic-induced supersensitivity of striatal dopamine receptors. Alteration of receptor site sensitivity may be a therapeutic goal. Pergolide, a direct acting dopamine agonist, decreased in guinea pigs haloperidol-induced increases in striatal dopamine receptor density both when coadministered and when given following haloperidol. Pergolide down-regulates supersensitive dopamine receptors and should be tested in the treatment of tardive dyskinesia.
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