期刊
NEUROTOXICITY RESEARCH
卷 29, 期 1, 页码 118-125出版社
SPRINGER
DOI: 10.1007/s12640-015-9566-4
关键词
Exercise; MPTP; Parkinson's disease; Cognition; Dopamine D2 receptor
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- CAPES-COFECUB (France/Brazil) [681/2010]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao de Apoio a Pesquisa Cientifica e Tecnologica do Estado de Santa Catarina (FAPESC)
The classical motor symptoms of Parkinson's disease (PD) are preceded by non-motor symptoms in preclinical stages, including cognition impairment. The current drug treatment for PD is palliative and does not meet the clinical challenges of the disease, such as levodopa-induced dyskinesia, non-motor symptoms, and neuroprotection. We investigated the neuroprotective and disease-modifying potential of physical exercise in a preclinical animal model of PD. C57BL/6 mice (adult males) ran on a horizontal treadmill for 6 weeks (moderate intensity, 5 times/week) and were treated intranasally with 65 mg/kg of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Exercise did not protect against MPTP-induced nigrostriatal neurodegeneration or frontostriatal dopamine depletion but decreased striatal dopamine turnover. Exercise also attenuated procedural and working memory impairment and D-2 receptor hypersensitivity in MPTP-treated mice. In summary, exercise improved dopaminergic neurotransmission and enhanced cognition in a preclinical animal model of PD.
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