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黑质纹状体多巴胺耗竭后丘脑板内核和运动丘脑生理学的改变。

Alterations in intralaminar and motor thalamic physiology following nigrostriatal dopamine depletion.

作者信息

Schneider J S, Rothblat D S

机构信息

Department of Neurobiology and Anatomy, MCP and Hahnemann University School of Medicine, Philadelphia, PA 19102, USA.

出版信息

Brain Res. 1996 Dec 2;742(1-2):25-33. doi: 10.1016/s0006-8993(96)00988-2.

DOI:10.1016/s0006-8993(96)00988-2
PMID:9117401
Abstract

The response of central median/central lateral (CM/CL) and ventral anterior/ventral lateral (VA/VL) thalamic neurons to tactile sensory stimulation of the face and electrical stimulation of the striatum was assessed in awake cats before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure. When cats exhibited Parkinson-like motor deficits, there was a significant decrease in the number of CM/CL and VA/VL neurons responsive to tactile stimulation of the face. Mean spontaneous firing rates decreased by 58% in the CM/CL nuclei, 65% in the VA, and 49% in the VL. The number of thalamic neurons responding to electrical stimulation of the striatum was also significantly decreased in parkinsonian animals. Approximately 6 weeks after MPTP exposure, when cats had spontaneously recovered gross motor function, thalamic responses to peripheral sensory stimulation, electrical stimulation of the CD, and spontaneous activity rates, returned to approximately normal levels in all thalamic areas studied. These findings support the concept that abnormalities in the transmission of information through the thalamus, and in particular, a decrease in sensory responsiveness in intralaminar and motor thalamic regions subsequent to nigrostriatal dopamine depletion, may contribute to the generation of Parkinson-like motor and sensorimotor deficits.

摘要

在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)暴露前后,对清醒猫中脑中央中核/中央外侧核(CM/CL)和丘脑腹前核/腹外侧核(VA/VL)神经元对面部触觉感觉刺激及纹状体电刺激的反应进行了评估。当猫出现帕金森样运动缺陷时,对脸部触觉刺激有反应的CM/CL和VA/VL神经元数量显著减少。CM/CL核的平均自发放电率下降了58%,VA下降了65%,VL下降了49%。在帕金森病动物中,对纹状体电刺激有反应的丘脑神经元数量也显著减少。MPTP暴露约6周后,当猫自发恢复了总体运动功能时,在所研究的所有丘脑区域,丘脑对周围感觉刺激、CD电刺激的反应以及自发放电率都恢复到了大致正常水平。这些发现支持这样一种观点,即通过丘脑的信息传递异常,特别是黑质纹状体多巴胺耗竭后丘脑板内核和运动丘脑区域感觉反应性降低,可能导致帕金森样运动和感觉运动缺陷的产生。

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