MISC

2002年6月

Brain-derived neurotrophic factor suppresses delayed apoptosis of oligodendrocytes after spinal cord injury in rats

JOURNAL OF NEUROTRAUMA
  • M Koda
  • ,
  • M Murakami
  • ,
  • H Ino
  • ,
  • K Yoshinaga
  • ,
  • O Ikeda
  • ,
  • M Hashimoto
  • ,
  • M Yamazaki
  • ,
  • C Nakayama
  • ,
  • H Moriya

19
6
開始ページ
777
終了ページ
785
記述言語
英語
掲載種別
DOI
10.1089/08977150260139147
出版者・発行元
MARY ANN LIEBERT INC PUBL

We evaluated the effect of brain-derived neurotrophic factor (BDNF) on cell death after spinal cord injury. A rat spinal cord injury model was produced by static load, and continuous intrathecal BDNF or vehicle infusion was carried out either immediately or 3 days after the injury. Cell death was examined by nuclear staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). After injury, typical apoptotic cells were observed. Double staining with TUNEL and specific cell markers revealed that, soon after the injury, the apoptotic or necrotic cells at the injury site were neurons and microglia. One week after the injury, apoptotic oligodendrocytes, but not apoptotic astrocytes, were observed in the white matter rostral and caudal to the injury site, whereas few apoptotic cells were found in the gray matter. The immediate BDNF treatment significantly reduced the number of TUNEL-positive cells in the adjacent rostral site I and 2 weeks after the injury, and in the adjacent caudal site 3 days and I week after the injury, even though there was no significant difference between BDNF-treated and control rats at the injury site itself. In addition, similar antiapoptotic effects were observed in these regions I week after injury in rats that received BDNF treatment from the third day after injury. These findings suggest that BDNF suppresses delayed apoptosis of oligodendrocytes after spinal cord injury, for which even delayed injections are effective. BDNF administration may therefore be useful for the clinical treatment of spinal cord injury through the suppression of secondary events.

リンク情報
DOI
https://doi.org/10.1089/08977150260139147
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000176588900008&DestApp=WOS_CPL
ID情報
  • DOI : 10.1089/08977150260139147
  • ISSN : 0897-7151
  • Web of Science ID : WOS:000176588900008

エクスポート
BibTeX RIS