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单侧颈内动脉注入1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)后,猴子出现偏侧帕金森综合征,这与纹状体多巴胺D2受体密度的同侧区域变化有关。

Hemiparkinsonism in a monkey after unilateral internal carotid artery infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is associated with regional ipsilateral changes in striatal dopamine D-2 receptor density.

作者信息

Joyce J N, Marshall J F, Bankiewicz K S, Kopin I J, Jacobowitz D M

出版信息

Brain Res. 1986 Sep 24;382(2):360-4. doi: 10.1016/0006-8993(86)91345-4.

DOI:10.1016/0006-8993(86)91345-4
PMID:2944565
Abstract

Infusion of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into the right internal carotid artery of a cynomologus monkey (Macaca fascicularis) induced an almost complete loss of the dopaminergic innervation of the right caudate-putamen and hemiparkinsonism. Digital subtraction autoradiography revealed that at 8 weeks postinjection, a major increase in [3H]spiroperidol binding to D-2 sites in the lateral regions of the right caudate nucleus and putamen occurred, without a significant change in the medial caudate nucleus and putamen. The 92-96% decrease in specific [3H]mazindol binding observed in the right striatum extended into the medial caudate nucleus and putamen and confirmed the extensive loss of dopamine inputs to this structure. The region of the increase in D-2 receptor density is innervated by somatosensory, motor and parietal cortex. This indicates that the increase in D-2 receptor density in this region of the striatum may play a particularly important role in the L-dihydroxyphenylanine-induced motoric recovery observed in such animals.

摘要

向食蟹猴(猕猴)的右侧颈内动脉注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)可导致右侧尾状核-壳核的多巴胺能神经支配几乎完全丧失,并引发偏侧帕金森病。数字减影放射自显影显示,注射后8周,右侧尾状核和壳核外侧区域与D-2位点结合的[3H]螺哌啶显著增加,而内侧尾状核和壳核无明显变化。在右侧纹状体中观察到的特异性[3H]马吲哚结合减少92 - 96%,这种减少延伸至内侧尾状核和壳核,证实了该结构的多巴胺输入大量丧失。D-2受体密度增加的区域接受体感、运动和顶叶皮质的神经支配。这表明纹状体该区域D-2受体密度的增加可能在这类动物中观察到的左旋多巴诱导的运动恢复中起特别重要的作用。

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