MODEL OF PARKINSON'S DISEASE

帕金森病模型

• 批准号: 3411738
• 负责人: GEORGE WAGNER
• 金额: $ 3.92万
• 依托单位: RUTGERS, THE STATE UNIV OF N.J.
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-04-01 至 1992-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3411738
• 关键词: Parkinson's disease; behavior; disease /disorder model; dopamine receptor; laboratory rat; model design /development; neurons; neurotoxins; sympathetic nervous system

The studies in this proposal are designed to determine if slight, presymptomatic lesions of the brain dopaminergic and/or serotonergic neurons can be assessed (i.e. unmasked) through the use of sensitive behavioral paradigms combined with drug challenge. Long-Evans rats will be used as subjects and they will be treated with the systemically administered neurotoxins 1- methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or methamphetamine. By varying the dose of these toxins, the magnitude of the lesion can be varied. The lesion magnitude for the dopaminergic system will range from 0% (i.e. control) to a maximum 75% depletion. These dopaminergic lesions will be accompanied by serotonergic lesions (simultaneously induced by both toxins) ranging in magnitude from 0% up to approximately 60% depletion. Both of these toxins have proven invaluable in advancing our understanding of the factors which lead to the degeneration of central dopaminergic and serotonergic neurons and, as such, have served as excellent models of Parkinson's disease. However, the use of rodents to explore these models has been somewhat restricted by the failure to demonstrate behavioral deficits associated with the toxin-induced damage. In this regard, however, the PI has obtained some degree of success stemming from use of carefully chosen behavioral paradigms used in conjunction with drug challenge tests. The demonstration that rodents with MPTP or methamphetamine-induced dopaminergic lesions do exhibit behavioral deficits has provided support for the validity of these models.

本提案中的研究旨在确定轻微的，

项目成果

The effects of deprenyl on methamphetamine-induced dopamine depletions.

丙炔苯丙胺对甲基苯丙胺引起的多巴胺消耗的影响。

• DOI: 10.1007/bf01245358
• 发表时间: 1992
• 期刊: Journal of neural transmission. General section
• 作者: Johnson,SK;Medina,D;Wagner,GC
• 通讯作者: Wagner,GC

Motor impairments after methamphetamine-induced neurotoxicity in the rat.

甲基苯丙胺诱导大鼠神经毒性后的运动障碍。

• 发表时间: 1992
• 期刊: The Journal of pharmacology and experimental therapeutics
• 作者: Walsh,SL;Wagner,GC
• 通讯作者: Wagner,GC

Functional consequences following methamphetamine-induced neuronal damage.

甲基苯丙胺引起的神经元损伤后的功能后果。

• DOI: 10.1007/bf00439543
• 发表时间: 1989
• 期刊: Psychopharmacology
• 影响因子: 3.4
• 作者: DeVito,MJ;Wagner,GC
• 通讯作者: Wagner,GC