NDLI: Dopamine D$_{2}$ agonist priming in intact and dopamine-lesioned rats

Content Provider	Springer Nature Link
Author	Kostrzewa, Richard M. Kostrzewa, John P. Nowak, Przemyslaw Kostrzewa, Rose Anna Brus, Ryszard
Copyright Year	2004
Abstract	Receptor priming is a recently discovered phenomenon by which receptor agonists produce abrupt and long-lived supersensitization of receptors. Induction of dopamine (DA) D2 receptor supersensitivity by the agonist quinpirole was discovered approximately 15 years ago, and was found to occur consistently if rats were treated repeatedly at daily or weekly or monthly intervals with low or high doses of quinpirole. In this review we summarize and discuss some of the major studies that underlie DA D2 receptor supersen-sitivity, describe behavioral processes that are known to be altered by DA D2 receptor supersensitivity, and discuss the importance of DA innervation on expression of enhanced behaviors. DA D2 receptor supersen-sitivity represents one of the neural mechanisms implicated in psychiatric disorders. Also, DA D$_{2}$ receptor supersensitivity and increased DA D$_{3}$ receptor expression are associated with motor dyskinesias, as in L-DOPA-treated Parkinson’s disease patients. An understanding of receptor priming, a knowledge of the types of behavioral expression associated with DA D$_{2}$ receptor supersensitivity, and an understanding of mechanisms associated with receptor supersen-sitization, can lead to improvements in the treatments of psychiatric and neurological disorders.
Starting Page	457
Ending Page	462
Page Count	6
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	6
Issue Number	6
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2004-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Dopamine Receptor supersensitivity Priming D$_{2}$ receptors Motor Dyskinesia Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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