Accumulating Microglia Phagocytose Injured Neurons in Hippocampal Slice Cultures : Involvement of p38 MAP Kinase

Katayama, Takahiro; Kobayashi, Hayato; Okamura, Toshiyuki; Yamasaki-Katayama, Yuko; Kibayashi, Tatsuya; Kimura, Hiroshi; Ohsawa, Keiko; Kohsaka, Shinichi; Minami, Masabumi

Accumulating Microglia Phagocytose Injured Neurons in Hippocampal Slice Cultures : Involvement of p38 MAP Kinase

Katayama, Takahiro; Kobayashi, Hayato; Okamura, Toshiyuki et al.

PLoS One, 2012, 7(7), e40813

Permalink : https://hdl.handle.net/2115/49841

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アクセス権	open access
URI	https://hdl.handle.net/2115/49841
タイトル	Accumulating Microglia Phagocytose Injured Neurons in Hippocampal Slice Cultures : Involvement of p38 MAP Kinase
著者	Katayama, Takahiro ; Kobayashi, Hayato ; Okamura, Toshiyuki ; Yamasaki-Katayama, Yuko ; Kibayashi, Tatsuya ; Kimura, Hiroshi ; Ohsawa, Keiko ; Kohsaka, Shinichi ; Minami, Masabumi
e-Rad_Researcher 90399957 著者名 Katayama, Takahiro
著者名 Kobayashi, Hayato
著者名 Okamura, Toshiyuki
著者名 Yamasaki-Katayama, Yuko
著者名 Kibayashi, Tatsuya
著者名 Kimura, Hiroshi
著者名 Ohsawa, Keiko
著者名 Kohsaka, Shinichi
e-Rad_Researcher 20243040 著者名 Minami, Masabumi
言語	英語
発行日	2012-07-17
出版者	Public Library of Science
収録物名	PLoS One
巻(号)	7(7)
ページ	e40813
抄録	In this study, microglial migration and phagocytosis were examined in mouse organotypic hippocampal slice cultures, which were treated with N-methyl-D-aspartate (NMDA) to selectively injure neuronal cells. Microglial cells were visualized by the expression of enhanced green fluorescent protein. Daily observation revealed microglial accumulation in the pyramidal cell layer, which peaked 5 to 6 days after NMDA treatment. Time-lapse imaging showed that microglia migrated to the pyramidal cell layer from adjacent and/or remote areas. There was no difference in the number of proliferating microglia between control and NMDA-treated slices in both the pyramidal cell layer and stratum radiatum, suggesting that microglial accumulation in the injured areas is mainly due to microglial migration, not to proliferation. Time-lapse imaging also showed that the injured neurons, which were visualized by propidium iodide (PI), disappeared just after being surrounded by microglia. Daily observation revealed that the intensity of PI fluorescence gradually attenuated, and this attenuation was suppressed by pretreatment with clodronate, a microglia toxin. These findings suggest that accumulating microglia phagocytosed injured neurons, and that PI fluorescence could be a useful indicator for microglial phagocytosis. Using this advantage to examine microglial phagocytosis in living slice cultures, we investigated the involvements of mitogen-activated protein (MAP) kinases in microglial accumulation and phagocytosis. p38 MAP kinase inhibitor SB203580, but not MAP kinase/extracellular signal-regulated kinase inhibitor PD98059 or c-Jun N-terminal kinase inhibitor SP600125, suppressed the attenuation of PI fluorescence. On the other hand, microglial accumulation in the injured areas was not inhibited by any of these inhibitors. These data suggest that p38 MAP kinase plays an important role in microglial phagocytosis of injured neurons.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
権利情報	Creative Commons Attribution 3.0 Unported
PISSN	1932-6203
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1371/journal.pone.0040813