DEGENERATION OF PYRAMIDAL PROJECTION NEURONS IN HUNTINGTONS-DISEASE CORTEX
DEGENERATION OF PYRAMIDAL PROJECTION NEURONS IN HUNTINGTONS-DISEASE CORTEX
复制标题
DOI：
10.1002/ana.410270217
复制
发表时间：
1990-02-01
影响因子：
11.2
通讯作者：
KOWALL, NW
中科院分区：
文献类型：
--
作者：
CUDKOWICZ, M;KOWALL, NW
我们检查了亨廷顿病患者和年龄匹配的对照受试者上额皮质中神经肽 Y 免疫反应性局部回路神经元和非磷酸化神经丝 (SMI 32) 免疫反应性锥体投射神经元的分布，以确定先前在亨廷顿病患者皮质中发现的神经肽 Y 增加和谷氨酸浓度降低的组织学对应物。我们发现亨廷顿病大脑和对照大脑中 SMI 32 免疫反应性神经元相对密度显着降低的区域中神经肽 Y 神经元的相对密度没有差异。动物研究表明，皮质局部回路神经元对 N-甲基-D-天冬氨酸型兴奋毒素（例如喹啉酸）有抵抗力。因此，患有亨廷顿病的大脑皮层神经肽 Y 神经元相对较少，可能是 N-甲基-D-天冬氨酸受体过度激活的结果。
We examined the distribution of neuropeptide Y immunoreactive local circuit neurons and nonphosphorylated neurofilament (SMI 32) immunoreactive pyramidal projection neurons in superior frontal cortex of patients with Huntington''s disease and age-matched control subjects to determine the histological counterpart of increased neuropeptide Y and decrease glutamate concentrations previously found in the cortex of patients with Huntington''s disease. We found no difference between the relative density of neuropeptide Y neurons in Huntington''s disease and control brains in regions where the relative density of SMI 32 immunoreactive neurons was significantly reduced. Animal studies show that cortical local circuit neurons are resistant to N-methyl-D-aspartate-type excitotoxins such as quinolinic acid. Relative sparing of neuropeptide Y neurons in cerebral cortex with Huntington''s disease may, therefore, be a result of excessive N-methyl-D-asparate receptor activation.