＜シンポジウム（3）―13―3＞脱髄性疾患の病態に基づいた新規治療戦略
光機能制御グリア細胞をもちいた神経修復・髄鞘再生戦略
澤田 誠
名古屋大学・環境医学研究所・脳機能分野〔〒464―8601 名古屋市千種区不老町〕
Microglia, macrophage-like cells in the CNS, are multi-functional cells; they play an important role in removal of dead cells or their remnants by phagocytosis in the CNS degeneration as well as are one of important cells in the CNS cytokine network. They are thought to be originated from mesoderm, and to be similar cells to other tissue-resident macrophages. As macrophages, activated microglia have been shown to remove potentially deleterious debris and promote tissue repair by secreting neurotrophic factors at the neuronal injury sites, however, they can release potentially cytotoxic substances in vitro, and at least so-called fully activated form of microglia which are observed at the injury site in AIDS dementia is neurotoxic. These suggest that some factor (s) may contribute to change microglial phenotype from protective to toxic, but the detail is not clear. Recently we generated channelrhodopsin-mutant protein expressing microglia, Ra2_GR and 6-3_GR. Channelrhodopsin is an ion channel activated by light irradiation. Intracellular sodium ion increased by light irradiation in both Ra2_GR and 6-3_GR accompanied by increase of mRNA expression such as pro-inflammatory cytokines, chemokines and iNOS. This technique can control microglial activation, therefore, it may provide a new strategy for repair/regeneration of neural and oligodendrocytic damages.
Full Text of this Article in Japanese PDF (415K)
(臨床神経, 52：1357−1359, 2012)
key words：ミクログリア，オリゴデンドロサイト前駆細胞，チャンネルロドプシン，オプトジェネティクス，光活性制御
（受付日：2012年5月25日）
