The Study Glial Regeneration and Neuroprotection on Brain Ischemic Model

脑缺血模型中胶质细胞再生及神经保护的研究

基本信息

批准号：
12672232
负责人：
TANIGUCHI Takashi
金额：
$ 1.92万
依托单位：
Kyoto Pharmaceutical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

It is known that occlusion of the middle cerebral artery (MCA) induces infarction and then neuronal loss and glial changes in the territory region of the MCA. α-Synuclein, a presynaptic protein, is markedly included in Lewy bodies (LB) in Parkinson's and LB diseases. We examined changes of α-synuclein after neurodegenerative insults such as MCA occlusion and KA injection, in comparison with MAP2 (a neuronal marker), CD11b (a microglial marker), GFAP (an astroglial marker) and HO-1 (a stress marker). After 2-h MCA occlusion and reperfusion, MAP2-immunoreactivity was markedly lost in the ipsilateral side of the striatum and cerebral cortex after 1 day. However, the immunoreactivities of α-synuclein did not markedly change even at 3 and 7 days after MCA occlusion, similar to after KA injection. Numerous CD11b-immunopositive microglia were observed in the regions (infarcted core) where MAP2 immunoreactivity was lost in the cerebral cortex and striatum, while GFAP-immunopositive astrocytes were activated in the border zones (perifocal regions). In addition, numerous MAP2-immunopositive glia-like cells were observed after MCA occlusion, suggesting that activated glial cells induced the phagocytosis of degenerating neurons. Thus, α-synuclein protein might not be scavenged by glial cells, although numerous neurons and dendrites are lost by neurodegenerative insults. Therefore, α-synuclein protein may readily condense in neurodegenerative regions.

众所周知，大脑中动脉 (MCA) 闭塞会诱发梗塞，然后导致 MCA 区域的神经元丢失和神经胶质变化，α-突触核蛋白（一种突触前蛋白）明显包含在帕金森病和帕金森病的路易体 (LB) 中。 LB 疾病。我们检查了神经退行性损伤（如 MCA 闭塞和 KA 注射）后 α-突触核蛋白的变化，并与 MAP2（神经元标记物）进行比较。 CD11b（小胶质细胞标记）、GFAP（星形胶质细胞标记）和 HO-1（应激标记）MCA 闭塞和再灌注 2 小时后，纹状体和大脑皮层的同侧 MAP2 免疫反应性在 1 小时后显着丧失。然而，即使在 MCA 闭塞后 3 和 7 天，α-突触核蛋白的免疫反应性也没有明显变化，与闭塞后类似。注射 KA 后，在大脑皮层和纹状体中 MAP2 免疫反应性丧失的区域（梗塞核心）观察到大量 CD11b 免疫阳性小胶质细胞，而在边缘区域（灶周区域）则激活了 GFAP 免疫阳性星形胶质细胞。 -MCA闭塞后观察到免疫阳性的胶质细胞样细胞，表明活化的胶质细胞诱导退化神经元的吞噬作用。因此，尽管神经退行性损伤导致大量神经元和树突损失，但α-突触核蛋白可能不会被神经胶质细胞清除。因此，α-突触核蛋白可能很容易在神经退行性区域中凝结。