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亨廷顿病患者额叶皮质 VI 层中[3H] 海人酸和[3H]α-氨基-3-羟基-5-甲基-4-异恶唑丙酸结合的选择性丧失

Selective loss of [3H]kainic acid and [3H]AMPA binding in layer VI of frontal cortex in Huntington's disease.

作者信息

Wagster M V, Hedreen J C, Peyser C E, Folstein S E, Ross C A

机构信息

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

出版信息

Exp Neurol. 1994 May;127(1):70-5. doi: 10.1006/exnr.1994.1081.

Abstract

Excitatory amino acid neurotoxicity has been proposed to cause the neostriatal neuronal degeneration of Huntington's disease (HD); N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and kainate receptors have been hypothesized to play important roles in this process. We have recently reported a loss of neurons in layer VI of the cerebral cortex in HD. Using quantitative autoradiographic methods, we have now measured NMDA, AMPA, and kainate receptor binding in the frontal cerebral cortex of the brains of controls and individuals with HD. We find no change in NMDA receptor binding but a selective decrease in kainate and AMPA receptor binding in layer VI. These data suggest that cerebral cortical neurons possessing kainate or AMPA receptors may be selectively vulnerable in individuals with HD.

摘要

兴奋性氨基酸神经毒性被认为可导致亨廷顿舞蹈症(HD)的新纹状体神经元变性;N-甲基-D-天冬氨酸(NMDA)、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)和海人藻酸受体被假定在这一过程中发挥重要作用。我们最近报道了HD患者大脑皮质第VI层神经元的缺失。利用定量放射自显影方法,我们现在测量了对照组和HD患者大脑额叶皮质中NMDA、AMPA和海人藻酸受体的结合情况。我们发现NMDA受体结合没有变化,但第VI层中海人藻酸和AMPA受体结合有选择性降低。这些数据表明,拥有海人藻酸或AMPA受体的大脑皮质神经元在HD患者中可能具有选择性易损性。

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