PMID- 12165137
OWN - NLM
STAT- MEDLINE
DCOM- 20020913
LR  - 20061115
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 19
IP  - 6
DP  - 2002 Jun
TI  - Brain-derived neurotrophic factor suppresses delayed apoptosis of 
      oligodendrocytes after spinal cord injury in rats.
PG  - 777-85
AB  - 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 1 and 2 weeks after the injury, and in the adjacent 
      caudal site 3 days and 1 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 
      1 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.
FAU - Koda, Masao
AU  - Koda M
AD  - Department of Orthopaedic Surgery, Chiba University Graduate School of Medicine, 
      Chiba, Japan. m-koda@nifty.com
FAU - Murakami, Masazumi
AU  - Murakami M
FAU - Ino, Hidetoshi
AU  - Ino H
FAU - Yoshinaga, Katsunori
AU  - Yoshinaga K
FAU - Ikeda, Osamu
AU  - Ikeda O
FAU - Hashimoto, Masayuki
AU  - Hashimoto M
FAU - Yamazaki, Masashi
AU  - Yamazaki M
FAU - Nakayama, Chikao
AU  - Nakayama C
FAU - Moriya, Hideshige
AU  - Moriya H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Oligodendroglia/*cytology/drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - Spinal Cord/pathology
MH  - Spinal Cord Injuries/*drug therapy/*pathology
EDAT- 2002/08/08 10:00
MHDA- 2002/09/14 10:01
CRDT- 2002/08/08 10:00
PHST- 2002/08/08 10:00 [pubmed]
PHST- 2002/09/14 10:01 [medline]
PHST- 2002/08/08 10:00 [entrez]
AID - 10.1089/08977150260139147 [doi]
PST - ppublish
SO  - J Neurotrauma. 2002 Jun;19(6):777-85. doi: 10.1089/08977150260139147.