期刊
NEUROBIOLOGY OF DISEASE
卷 35, 期 3, 页码 376-384出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.05.019
关键词
Levodopa; Quinpirole; Striatum; Electrophysiology; Dopamine; Parkinson's disease; Striatonigral; Striatopallidal; GABA interneuron
资金
- Centre National de la Recherche Scientifique
- University of Bordeaux and 'La Fondation de France'
- Secretaria de Ciencia, Tecnologia e Innovacion Productiva
- Fondo para la Investigacion Cientifica y Tecnologica [PICT 26323]
- Universidad de Buenos Aires and Consejo Nacional de Investigaciones Cientificas y Tecnicas (Argentina)
- International Cooperation Program SECyT-ECOS [A05S01]
In Parkinson's disease dopamine depletion imbalances the two major output pathways of the striatum. L-DOPA replacement therapy is believed to correct this imbalance by providing effective D1 and D2 receptor stimulation to striatonigral and striatopallidal neurons, respectively. Here we tested this assumption in the rat model of Parkinsonism by monitoring the spike response of identified striatal neurons to cortical stimulation. As predicted, in 6-hydroxydopamine lesioned rats we observed that L-DOPA (6 mg/kg + benserazide), apomorphine and the D2 agonist quinpirole (0.5 mg/kg i.p.) counteract the enhanced responsiveness of striatopallidal neurons. Unexpectedly, the depressed responsiveness of striatonigral neurons was corrected by quinpirole whereas D1 stimulation exerted no (apomorphine, cPB) or worsening effects (L-DOPA, SKF38393 10 mg/kg). Therefore, quinpirole, but not D1 stimulation, restores functional equilibrium between the two striatal output pathways. Our results might explain the therapeutic effect of D2-based medications in Parkinson's disease. (C) 2009 Elsevier Inc. All rights reserved.
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