Cho Byung Pil, Sugama Shuei, Shin Dong Hoon, DeGiorgio Lorraine A, Kim Sung Soo, Kim Yoon Seong, Lim So Young, Park Key Chung, Volpe Bruce T, Cho Sunghee, Joh Tong H
The Burke Medical Research Institute, Department of Neurology and Neuroscience, Weill Medical College, Graduate School of Medical Sciences of Cornell University, White Plains, New York 10605, USA.
Cell Mol Neurobiol. 2003 Oct;23(4-5):551-60. doi: 10.1023/a:1025024129946.
Transection of the medial forebrain bundle caused apoptosis of dopamine neurons in the rat substantia nigra. Immunohistochemical localization of activated microglia and tyrosine hydroxylase in the axotomized substantia nigra showed that activation of microglia was rapid and OX-6 (MHC-II marker)-positive and ED1 (lysosomal phagocytic marker)-positive microglia were apposed to structurally intact tyrosine hydroxylase-positive dopamine neurons, indicating microglial phagocytosis of degenerating dopamine neurons. The occurrence of microglial phagocytosis at early stages of apoptosis may indicate the evolution of apoptosis into an irreversible state. Alternatively, interventions that suppress early activation of microglia might lead to novel mechanisms for neuron protection.
内侧前脑束横断导致大鼠黑质中多巴胺能神经元凋亡。对轴突切断的黑质中活化小胶质细胞和酪氨酸羟化酶进行免疫组织化学定位显示,小胶质细胞的活化迅速,OX-6(主要组织相容性复合体II类标志物)阳性和ED1(溶酶体吞噬标志物)阳性的小胶质细胞与结构完整的酪氨酸羟化酶阳性多巴胺能神经元相邻,表明小胶质细胞对退化的多巴胺能神经元进行吞噬。凋亡早期小胶质细胞吞噬作用的发生可能表明凋亡已发展到不可逆状态。或者,抑制小胶质细胞早期活化的干预措施可能会带来新的神经元保护机制。