MISC

2012年11月

Differential responses of endogenous adult mouse neural precursors to excess neuronal excitation

EUROPEAN JOURNAL OF NEUROSCIENCE
  • Tetsuji Mori
  • ,
  • Taketoshi Wakabayashi
  • ,
  • Yukie Hirahara
  • ,
  • Yasuharu Takamori
  • ,
  • Taro Koike
  • ,
  • Kiyoshi Kurokawa
  • ,
  • Hisao Yamada

36
9
開始ページ
3184
終了ページ
3193
記述言語
英語
掲載種別
DOI
10.1111/j.1460-9568.2012.08244.x
出版者・発行元
WILEY-BLACKWELL

Adult neurogenesis in the subgranular zone of the hippocampus (SGZ) is enhanced by excess as well as mild neuronal excitation, such as chemoconvulsant-induced brief seizures. Because most studies of neurogenesis after seizures have focused on the SGZ, the threshold of neuronal excitation required to enhance neurogenesis in the subventricular zone (SVZ) is not clear. Therefore, we examined the responses of SVZ precursors to brief generalized clonic seizures induced by a single administration of the chemoconvulsant pentylenetetrazole (PTZ). Cell cycle progression of precursors was analysed by systemic administration of thymidine analogues. We found that brief seizures immediately resulted in cell cycle retardation in the SVZ. However, the same effect was not seen in the SGZ. This initial cell cycle retardation in the SVZ was followed by enhanced cell cycle re-entry after the first round of mitosis, leading to precursor pool expansion, but the cell cycle retardation and expansion of the precursor pool were transient. Cell cycle progression in the PTZ-treated group returned to normal after one cell cycle. The numbers of precursors in the SVZ and new neurons in the olfactory bulb, which are descendants of SVZ precursors, were not significantly different from those in control mice more than 2 days after seizures. Because similar effects were observed following electroconvulsive seizures, these responses are likely to be general effects of brief seizures. These results suggest that neurogenesis in the SVZ is more tightly regulated and requires stronger stimuli to be modified than that in the SGZ.

リンク情報
DOI
https://doi.org/10.1111/j.1460-9568.2012.08244.x
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000310683800005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/j.1460-9568.2012.08244.x
  • ISSN : 0953-816X
  • Web of Science ID : WOS:000310683800005

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