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介导1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的猴子帕金森病的神经机制:2-脱氧葡萄糖摄取所提示的纹状体苍白球和纹状体黑质通路的相对作用

Neural mechanisms mediating 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine-induced parkinsonism in the monkey: relative contributions of the striatopallidal and striatonigral pathways as suggested by 2-deoxyglucose uptake.

作者信息

Mitchell I J, Cross A J, Sambrook M A, Crossman A R

出版信息

Neurosci Lett. 1986 Jan 2;63(1):61-5. doi: 10.1016/0304-3940(86)90013-3.

Abstract

The neural mechanisms which mediate parkinsonian symptoms have been investigated in the monkey by application of the 2-deoxyglucose (2-DG) metabolic mapping technique to animals rendered parkinsonian by systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results show that 2-DG uptake was dramatically increased in the globus pallidus, but not the substantia nigra pars reticulata, in parkinsonian monkeys compared to controls. This observation has been interpreted as indicating increased synaptic activity in the putaminopallidal, but not the caudatonigral, pathway which suggests a relatively greater involvement of the putaminopallidal pathway in relation to the motor manifestations of parkinsonism.

摘要

通过将2-脱氧葡萄糖(2-DG)代谢图谱技术应用于经全身给予1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)而患帕金森病的猴子,对介导帕金森病症状的神经机制进行了研究。结果显示,与对照组相比,帕金森病猴子苍白球中的2-DG摄取显著增加,而黑质网状部则未增加。这一观察结果被解释为表明壳核-苍白球通路而非尾状核-黑质通路的突触活动增加,这表明壳核-苍白球通路在帕金森病运动表现方面的参与程度相对更高。

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