NMDA receptor losses in putamen from patients with Huntington's disease.
NMDA receptor losses in putamen from patients with Huntington's disease.
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DOI：
10.1126/science.2841762
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发表时间：
1988-08
期刊：
影响因子：
56.9
通讯作者：
Anne B. Young;J. Greenamyre;Z. Hollingsworth;R. Albin;Constance J. D'Amato;Ira Shoulson;J. Penney
中科院分区：
文献类型：
--
作者：
Anne B. Young;J. Greenamyre;Z. Hollingsworth;R. Albin;Constance J. D'Amato;Ira Shoulson;J. Penney
在患有亨廷顿病（HD）的个体的壳核和大脑皮层中，将N-甲基-D-天冬氨酸（NMDA）、苯环利定（PCP）和使君子酸受体结合与苯二氮卓类、γ-氨基丁酸（GABA）和毒蕈碱胆碱能受体结合进行比较。与正常大脑中的结合相比，HD大脑中壳核中的NMDA受体结合减少了93%。使君子酸和PCP受体的结合减少了67%，与其他受体的结合减少了55%或更少。在HD大脑中，与大脑皮层中这些受体的结合没有变化。结果支持NMDA受体介导的神经毒性在亨廷顿病的病理生理学中起作用的假设。
N-Methyl-D-aspartate (NMDA), phencyclidine (PCP), and quisqualate receptor binding were compared to benzodiazepine, gamma-aminobutyric acid (GABA), and muscarinic cholinergic receptor binding in the putamen and cerebral cortex of individuals with Huntington's disease (HD). NMDA receptor binding was reduced by 93 percent in putamen from HD brains compared to binding in normal brains. Quisqualate and PCP receptor binding were reduced by 67 percent, and the binding to other receptors was reduced by 55 percent or less. Binding to these receptors in the cerebral cortex was unchanged in HD brains. The results support the hypothesis that NMDA receptor-mediated neurotoxicity plays a role in the pathophysiology of Huntington's disease.