ナカムラ ノブヒロ   NAKAMURA NOBUHIRO
  中村 暢宏
   所属   京都産業大学  生命科学部 先端生命科学科
   職種   教授
言語種別 英語
発行・発表の年月 2008
形態種別 研究論文
査読 査読あり
標題 Insensitivity to glutamate neurotoxicity mediated by NMDA receptors in association with delayed mitochondrial membrane potential disruption in cultured rat cortical neurons
執筆形態 その他
掲載誌名 Journal of Neurochemistry
出版社・発行元 WILEY-BLACKWELL
巻・号・頁 105(5),pp.1886-1900
著者・共著者 Kambe, Y.,Nakamichi, N.,Georgiev, D.D.,Nakamura, N.,Taniura, H.,Yoneda, Y.
概要 We have attempted to elucidate mechanisms underlying differential vulnerability to glutamate (Glu) using cultured neurons prepared from discrete structures of embryonic rat brains. Brief exposure to Glu led to a significant decrease in the mitochondrial activity in hippocampal neurons cultured for 9 or 12 days at 10 mu M to 1 mM with an apoptosis-like profile, without markedly affecting that in cortical neurons. Brief exposure to Glu also increased lactate dehydrogenase release along with a marked decrease in the number of cells immunoreactive for a neuronal marker protein in hippocampal, but not cortical, neurons. Similar insensitivity was seen to the cytotoxicity by NMDA, but not to that by tunicamycin, 2,4-dinitrophenol, hydrogen peroxide or A23187, in cortical neurons. However, NMDA was more efficient in increasing intracellular free Ca(2+) levels in cortical neurons than in hippocampal neurons. Antagonists for neuroprotective metabotropic Glu receptors failed to significantly affect the insensitivity to Glu, while NMDA was more effective in disrupting mitochondrial membrane potentials in hippocampal than cortical neurons. These results suggest that cortical neurons would be insensitive to the apoptotic neurotoxicity mediated by NMDA receptors through a mechanism related to mitochondrial membrane potentials, rather than intracellular free Ca(2+) levels, in the rat brain.
DOI 10.1111/j.1471-4159.2008.05270.x
ISSN 0022-3042
Put Code(ORCID) 19809401