位置，位置，位置：突触和 extrasynaptic NMDA 受体在亨廷顿病中的对比作用。
Location, location, location: contrasting roles of synaptic and extrasynaptic NMDA receptors in Huntington's disease.
机构信息
Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, Los Angeles, CA 90095, USA.
出版信息
Neuron. 2010 Jan 28;65(2):145-7. doi: 10.1016/j.neuron.2010.01.010.
Abstract
Abnormally enhanced N-methyl-D-aspartate (NMDA) receptor function is implicated in Huntington's disease (HD). In this issue of Neuron and a recent issue of Nature Medicine, an abnormal balance between the activity of NMDA receptors at synaptic (prosurvival) and extrasynaptic (proapoptotic) sites has been uncovered in a cellular and a mouse model of HD.
摘要
异常增强的 N-甲基-D-天冬氨酸（NMDA）受体功能与亨廷顿病（HD）有关。在本期《神经元》和最近一期《自然医学》中，在 HD 的细胞和小鼠模型中发现了 NMDA 受体在突触（生存促进）和突触外（促凋亡）部位的活性之间存在异常平衡。
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本文引用的文献
1
Early increase in extrasynaptic NMDA receptor signaling and expression contributes to phenotype onset in Huntington's disease mice.早期 extrasynaptic NMDA 受体信号和表达的增加导致亨廷顿病小鼠表型的出现。
Neuron. 2010 Jan 28;65(2):178-90. doi: 10.1016/j.neuron.2010.01.008.
2
Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin.突触与突触外NMDA受体活性之间的平衡影响突变型亨廷顿蛋白的包涵体形成和神经毒性。
Nat Med. 2009 Dec;15(12):1407-13. doi: 10.1038/nm.2056. Epub 2009 Nov 15.
3
Alterations in cortical excitation and inhibition in genetic mouse models of Huntington's disease.亨廷顿舞蹈症基因小鼠模型中皮质兴奋与抑制的改变
J Neurosci. 2009 Aug 19;29(33):10371-86. doi: 10.1523/JNEUROSCI.1592-09.2009.
4
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Science. 2009 Jun 5;324(5932):1327-30. doi: 10.1126/science.1172871.
5
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J Neurosci. 2009 Feb 25;29(8):2414-27. doi: 10.1523/JNEUROSCI.5687-08.2009.
6
The dichotomy of NMDA receptor signaling.NMDA受体信号传导的二分法。
Neuroscientist. 2007 Dec;13(6):572-9. doi: 10.1177/10738584070130060401.
7
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8
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9
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Parkinsonism Relat Disord. 2007 Oct;13(7):453-4. doi: 10.1016/j.parkreldis.2006.08.005. Epub 2006 Oct 13.
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