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.
AuthorsS Chiu, C S Paulose, R K Mishra
JournalScience (New York, N.Y.) (Science) Vol. 214 Issue 4526 Pg. 1261-2 (Dec 11 1981) ISSN: 0036-8075 [Print] UNITED STATES
PMID6117947 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Butyrophenones
  • Receptors, Dopamine
  • Spiperone
  • MSH Release-Inhibiting Hormone
  • Haloperidol
  • Chlorpromazine
  • Animals
  • Butyrophenones (metabolism)
  • Chlorpromazine (pharmacology)
  • Corpus Striatum (metabolism)
  • Haloperidol (pharmacology)
  • Kinetics
  • MSH Release-Inhibiting Hormone (pharmacology)
  • Male
  • Rats
  • Rats, Inbred Strains
  • Receptors, Dopamine (drug effects, metabolism)
  • Spiperone (metabolism)

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