HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Faculty of Pharmaceutical Sciences >
Peer-reviewed Journal Articles, etc >

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

This item is licensed under:Creative Commons Attribution 3.0 Unported

Files in This Item:
PLo7-7_e40813.pdf8 MBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Accumulating Microglia Phagocytose Injured Neurons in Hippocampal Slice Cultures : Involvement of p38 MAP Kinase
Authors: Katayama, Takahiro Browse this author →KAKEN DB
Kobayashi, Hayato Browse this author
Okamura, Toshiyuki Browse this author
Yamasaki-Katayama, Yuko Browse this author
Kibayashi, Tatsuya Browse this author
Kimura, Hiroshi Browse this author
Ohsawa, Keiko Browse this author
Kohsaka, Shinichi Browse this author
Minami, Masabumi Browse this author →KAKEN DB
Issue Date: 17-Jul-2012
Publisher: Public Library of Science
Journal Title: PLoS One
Volume: 7
Issue: 7
Start Page: e40813
Publisher DOI: 10.1371/journal.pone.0040813
Abstract: 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.
Type: article
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 南 雅文

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 - Hokkaido University