Hasegawa Sanae, Yamaguchi Masahiro, Nagao Hiroshi, Mishina Masayoshi, Mori Kensaku
Department of Physiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
J Neuroimmunol. 2007 May;186(1-2):75-85. doi: 10.1016/j.jneuroim.2007.03.005. Epub 2007 Apr 10.
Microglia participate in immune responses in the brain. However, little is known about the contact-mediated interaction between microglia and neurons. We report here that the cell-to-cell contacts between microglial processes and dendrites of hippocampal CA1 neurons were dramatically increased in density and area following local injection of kainic acid (KA). A similar KA-induced increase in the degree of intercellular contacts was observed in mice lacking telencephalin (TLCN), a neuronal dendritic adhesion molecule of ICAM family. The results suggest that adhesive contacts independent of TLCN and contact-mediated interactions between microglia and dendrites were promoted by excitotoxic brain injury.
小胶质细胞参与大脑中的免疫反应。然而，关于小胶质细胞与神经元之间接触介导的相互作用却知之甚少。我们在此报告，在局部注射海藻酸（KA）后，小胶质细胞突起与海马CA1神经元树突之间的细胞间接触在密度和面积上显著增加。在缺乏端脑素（TLCN）的小鼠中也观察到了类似的KA诱导的细胞间接触程度增加，TLCN是ICAM家族的一种神经元树突粘附分子。结果表明，兴奋性毒性脑损伤促进了独立于TLCN的粘附接触以及小胶质细胞与树突之间的接触介导的相互作用。
