The effect of dopamine on MPTP-induced rotarod disability

被引：28

作者：

Ayton, Scott ^{[1
]}

George, Jessica L. ^{[1
]}

Adlard, Paul A. ^{[1
]}

Bush, Ashley I. ^{[1
]}

Cherny, Robert A. ^{[1
]}

Finkelstein, David I. ^{[1
]}

机构：

[1] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia

来源：

NEUROSCIENCE LETTERS | 2013年 / 543卷

基金：

澳大利亚研究理事会; 英国医学研究理事会;

关键词：

Parkinson's disease; MPTP; Dopamine; Rotarod; PARKINSONS-DISEASE; MOUSE MODEL; INDUCED DYSKINESIA; SUBSTANTIA-NIGRA; MICE; MOTOR; NEUROTOXICITY; BEHAVIOR; EXTRACT; NEURONS;

D O I：

10.1016/j.neulet.2013.02.066

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Dopamine depletion in Parkinson's disease (PD) results in bradykinesia and tremor. Therapeutic administration of the dopamine precursor, L-Dopa, alleviates these symptoms but dyskinesia's can manifest with chronic treatment. In the MPTP toxin mouse model of PD, lesion severity is often assessed by the rotarod behavioral assay. Dopamine depletion by MPTP is thought to induce rotarod behavioral decline. Here we surveyed rotarod behavior and striatal dopamine at timed intervals post-MPTP. Paradoxically, rotarod disability coincided with gradual striatal dopamine restoration. L-Dopa supplementation exacerbated rotarod disability, whereas dopamine antagonism restored performance. Conclusion: dopamine restoration, not depletion, precipitates rotarod disability after MPTP intoxication, and caution should be applied when using this assay for MPTP. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

引用

页码：105 / 109

页数：5

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