Neuroleptic drug-induced dopamine receptor supersensitivity: antagonism by L-prolyl-L-leucyl-glycinamide.
An animal model of tardive dyskinesia was used to evaluate the potential antidyskinetic properties of the neuropeptide L-prolyl-L-leucyl-glycinamide (PLG). In rats, PLG administered concurrently with the neuroleptic drug haloperidol or chlorpromazine antagonized the enhancement of specific [3H]spiroperidol binding in the striatum that is associated with long-term neuroleptic treatment. The results are discussed in relation to a possible functional coupling of the putative PLG receptor with neuroleptic-dopamine receptor complex and clinical implications for tardive dyskinesia.
D000818:Animals; D002090:Butyrophenones / Q000378:metabolism*; D002746:Chlorpromazine / Q000494:pharmacology*; D003342:Corpus Striatum / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology*; D007700:Kinetics; D009075:MSH Release-Inhibiting Hormone / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000378:metabolism*; D013134:Spiperone / Q000378:metabolism*
D002090:Butyrophenones; D011954:Receptors, Dopamine; D013134:Spiperone; D009075:MSH Release-Inhibiting Hormone; D006220:Haloperidol; D002746:Chlorpromazine