Mesolimbic and striatal dopamine receptor supersensitivity: Prophylactic and reversal effects of L-prolyl-L-leucyl-glycinamide (PLG)

Pauline Chiu; G. Rajakumar; Simon Chiu; Rodney L. Johnson; Ram K. Mishra

doi:10.1016/0196-9781(85)90036-1

Mesolimbic and striatal dopamine receptor supersensitivity: Prophylactic and reversal effects of L-prolyl-L-leucyl-glycinamide (PLG)

Pauline Chiu, G. Rajakumar, Simon Chiu, Rodney L. Johnson, Ram K. Mishra

Research output: Contribution to journal › Article › peer-review

32 Scopus citations

Abstract

Functional supersensitivity of mesolimbic and striatal dopamine receptors has been suggested to contribute to the pathogenesis of schizophrenia and tardive dyskinesia. Using the rodent model of chronic administration of the neuroleptic haloperidol, we investigated the possible desensitizing effects of a tripeptide structurally unrelated to dopamine agonists, L-prolyl-L-leucyl-glycinamide (PLG) on mesolimbic and striatal dopaminergic receptor supersensitivity. Administration of PLG either prior to or after chronic haloperidol, inhibited the supersensitivity of dopamine receptors. The results have implications for pharmacological intervention in preventing tardive dyskinesia and relapse psychosis of schizophrenia.

Original language	English (US)
Pages (from-to)	179-183
Number of pages	5
Journal	Peptides
Volume	6
Issue number	2
DOIs	https://doi.org/10.1016/0196-9781(85)90036-1
State	Published - 1985
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by the Ontario Mental Health Foundation of Canada and the National Institute of Neurological and Communicative Disorders and Stroke, NIH, USA. We wish to thank Sara DeSilvio for skillfully typing the manuscript.

Keywords

Haloperidol
Mesolimbic and striatal dopamine receptors
PLG
Supersensitivity
Tardive dyskinesia

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title = "Mesolimbic and striatal dopamine receptor supersensitivity: Prophylactic and reversal effects of L-prolyl-L-leucyl-glycinamide (PLG)",

abstract = "Functional supersensitivity of mesolimbic and striatal dopamine receptors has been suggested to contribute to the pathogenesis of schizophrenia and tardive dyskinesia. Using the rodent model of chronic administration of the neuroleptic haloperidol, we investigated the possible desensitizing effects of a tripeptide structurally unrelated to dopamine agonists, L-prolyl-L-leucyl-glycinamide (PLG) on mesolimbic and striatal dopaminergic receptor supersensitivity. Administration of PLG either prior to or after chronic haloperidol, inhibited the supersensitivity of dopamine receptors. The results have implications for pharmacological intervention in preventing tardive dyskinesia and relapse psychosis of schizophrenia.",

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author = "Pauline Chiu and G. Rajakumar and Simon Chiu and Johnson, {Rodney L.} and Mishra, {Ram K.}",

note = "Funding Information: This study was supported by the Ontario Mental Health Foundation of Canada and the National Institute of Neurological and Communicative Disorders and Stroke, NIH, USA. We wish to thank Sara DeSilvio for skillfully typing the manuscript.",

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AU - Chiu, Pauline

AU - Rajakumar, G.

AU - Chiu, Simon

AU - Johnson, Rodney L.

AU - Mishra, Ram K.

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AB - Functional supersensitivity of mesolimbic and striatal dopamine receptors has been suggested to contribute to the pathogenesis of schizophrenia and tardive dyskinesia. Using the rodent model of chronic administration of the neuroleptic haloperidol, we investigated the possible desensitizing effects of a tripeptide structurally unrelated to dopamine agonists, L-prolyl-L-leucyl-glycinamide (PLG) on mesolimbic and striatal dopaminergic receptor supersensitivity. Administration of PLG either prior to or after chronic haloperidol, inhibited the supersensitivity of dopamine receptors. The results have implications for pharmacological intervention in preventing tardive dyskinesia and relapse psychosis of schizophrenia.

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Mesolimbic and striatal dopamine receptor supersensitivity: Prophylactic and reversal effects of L-prolyl-L-leucyl-glycinamide (PLG)

Abstract

Bibliographical note

Keywords

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