Neurodegeneration of substantia nigra accompanied with macrophage/microglia infiltration after intrastriatal hemorrhage
Neurodegeneration of substantia nigra accompanied with macrophage/microglia infiltration after intrastriatal hemorrhage
复制标题
DOI：
10.1016/s0168-0102(03)00065-8
复制
发表时间：
2003-07-01
影响因子：
2.9
通讯作者：
Yamada, K
中科院分区：
文献类型：
--
作者：
Imamura, N;Hida, H;Yamada, K
大鼠纹状体内出血导致黑质（SN）神经变性，随后出现ED 1（+）细胞（巨噬细胞/小胶质细胞）。出血后至少8周可观察到ED 1（+）细胞。在ED 1（+）细胞中，p38丝裂原活化蛋白激酶（MAPK）磷酸化，同时表达脑源性神经营养因子（BDNF）mRNA和BDNF，提示激活的p38 MAPK（+）/ED 1（+）细胞可产生BDNF，对黑质变性神经元具有营养作用。而ELISA检测结果显示，出血后7天，同侧黑质BDNF蛋白表达明显减少，这可能是由于丘脑腹外侧部BDNF免疫反应阳性神经元数量减少所致。数据表明，出血后浸润同侧黑质的ED 1（+）细胞中p38 MAPK的激活可能产生BDNF，但ED 1（+）细胞产生的BDNF量不足以拯救变性神经元。(C)2003年爱思唯尔科学爱尔兰有限公司和日本神经科学学会。All rights reserved.
Intrastriatal hemorrhage in rats causes neurodegenaration of the substantia nigra (SN) followed by the appearance of ED1(+) cells (macrophage/microglia). ED1(+) cells were observed for at least 8 weeks after hemorrhage. Phosphorylation of p38 mitogen-activated protein kinase (MAPK) was shown in ED1(+) cells with the expression of both brain-derived neurotrophic factor (BDNF) mRNA and BDNF, suggesting that activated-p38 MAPK(+)/ED1(+) cells would produce BDNF and may exhibit trophic effect on the degenerating neurons in the SN. However, in ELISA, BDNF protein decreased significantly in ipsilateral SN at 7 days after hemorrhage, which may be due to a dramatic decrease of BDNF immunoreactive neurons in pars compacta. Data suggest that activation of p38 MAPK in ED1(+) cells infiltrating in ipsilateral SN after hemorrhage may produce BDNF, but that the amount of BDNF produced from ED1(+) cells is insufficient for the rescue of degenerating neurons. (C) 2003 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved.