論文

査読有り
2005年7月

Critical period for sensory experience-dependent survival of newly generated granule cells in the adult mouse olfactory bulb

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
  • M Yamaguchi
  • ,
  • K Mori

102
27
開始ページ
9697
終了ページ
9702
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1073/pnas.0406082102
出版者・発行元
NATL ACAD SCIENCES

Granule cells in the olfactory bulb (OB) are continually produced and added into the neuronal circuit in the adult brain. Sensory input to the OB plays a key role in the survival of newly generated granule cells. Here, we examined in the adult mice whether there is a time window after the generation of new granule cells when their survival is strongly influenced by sensory input. New granule cells were labeled by BrdUrd injection, and the mice were deprived of sensory input unilaterally by naris cauterization. During the initial 14 days after BrdUrd labeling, the number of BrdUrd-positive granule cells was similar for deprived and undeprived OBs. At 28 days or later, the BrdUrd-positive cell number remarkably decreased in the deprived OB. Cauterization at days 14-28 effectively reduced the number of BrdUrd-positive granule cells, whereas 2-week cauterization before or after this period produced little effect. Administration of diazepam, a GABA(A) receptor modulator, decreased the number of BrdUrd-positive granule cells. The diazepam administration was most effective at days 14-28. Histochemical examination showed that activation of caspase-3 was accompanied by apoptotic cell death of granule cells that was induced by sensory deprivation or diazepam administration. Double labeling with activated caspase-3 and BrdUrd indicated that granule cells at days 14-20 were most susceptible to cell death. These results indicate that there is a critical period when the survival of new granule cells is determined in a sensory experience-dependent manner and that the pharmacological manipulation can mimic the effect of sensory deprivation.

リンク情報
DOI
https://doi.org/10.1073/pnas.0406082102
CiNii Articles
http://ci.nii.ac.jp/naid/80017438187
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15976032
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000230406000046&DestApp=WOS_CPL
ID情報
  • DOI : 10.1073/pnas.0406082102
  • ISSN : 0027-8424
  • CiNii Articles ID : 80017438187
  • PubMed ID : 15976032
  • Web of Science ID : WOS:000230406000046

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