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纹状体能量代谢的抑制会导致同侧黑质细胞丢失。

Inhibition of striatal energy metabolism produces cell loss in the ipsilateral substantia nigra.

作者信息

Sonsalla P K, Manzino L, Sinton C M, Liang C L, German D C, Zeevalk G D

机构信息

University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Department of Neurology, Piscataway 08854, USA.

出版信息

Brain Res. 1997 Oct 31;773(1-2):223-6. doi: 10.1016/s0006-8993(97)00941-4.

DOI:10.1016/s0006-8993(97)00941-4
PMID:9409726
Abstract

This study examined whether damage to dopamine (DA) nerve terminals via inhibition of energy metabolism in the striatum would result in the retrograde loss of cell bodies in the substantia nigra. Infusion of 2 micromol malonate into the left striatum of rats resulted in a 67% loss of striatal DA and a 40% loss of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra. No change in the number of Nissl-positive-TH-negative neurons was observed. These findings demonstrate the retrograde destruction of DA cell bodies in the substantia nigra resulting from energy impairment at their terminal projection site.

摘要

本研究检测了通过抑制纹状体中的能量代谢对多巴胺(DA)神经末梢造成损伤是否会导致黑质中细胞体的逆行性丢失。向大鼠左侧纹状体注入2微摩尔丙二酸,导致纹状体DA减少67%,黑质中酪氨酸羟化酶(TH)阳性神经元减少40%。未观察到尼氏染色阳性-TH阴性神经元数量的变化。这些发现表明,由于其终末投射部位的能量损伤,导致黑质中DA细胞体发生逆行性破坏。

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Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion.部分线粒体抑制通过过氧化氢水平升高而非ATP耗竭导致纹状体多巴胺释放抑制和中等棘状神经元去极化。
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