帕金森病的黑质网状部神经元

Hardman C.D. , McRitchie D.A. , Halliday G.M. , Cartwright H.R. , Morris J.G.L.
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引用次数: 58

摘要

我们通过免疫组织化学检查了帕金森病患者和年龄匹配对照中含有小蛋白的黑质神经元。小白蛋白是一种钙结合蛋白,参与细胞内钙的缓冲,在本研究中,它定位于人类网状部的大多数非色素神经元中。先前的研究表明,网状部小蛋白免疫反应神经元是gaba能神经元,并投射到运动丘脑和顶盖。由于帕金森氏症中多巴胺能抑制的丧失,它们的输出增加,通过丘脑通路减少皮层的激活,导致帕金森氏症症状。在帕金森氏症中,这些神经元的细小蛋白免疫反应性明显丧失,尽管没有证据表明实际的细胞丧失。这种小蛋白免疫反应性的丧失仅在终末期帕金森病患者中检测到。
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Substantia Nigra Pars Reticulata Neurons in Parkinson's Disease

We have examined by immunohistochemistry the parvalbumin-containing neurons of the substantia nigra in patients with Parkinson's disease and in age-matched controls. Parvalbumin, a calcium binding protein, is involved in buffering intracellular calcium and in this study was localized within the majority of non-pigmented neurons of the human pars reticulata. Previous studies have shown that the parvalbumin-immunoreactive pars reticulata neurons are GABAergic and project to the motor thalamus and tectum. Their increased output, due to the loss of dopaminergic inhibition in Parkinson's disease, decreases cortical activation via thalamic pathways, causing parkinsonian symptoms. In Parkinson's disease there was a significant loss of parvalbumin-immunoreactivity from these neurons, though there was no evidence of actual cell loss. This loss of parvalbumin-immunoreactivity was detected only in those cases with end-stage Parkinson's disease.

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