PMID- 12470870
OWN - NLM
STAT- MEDLINE
DCOM- 20030327
LR  - 20220330
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 958
IP  - 2
DP  - 2002 Dec 27
TI  - Involvement of a spinal brain-derived neurotrophic factor/full-length TrkB 
      pathway in the development of nerve injury-induced thermal hyperalgesia in mice.
PG  - 338-46
AB  - Partial sciatic nerve ligation in mice caused a marked and persistent decrease in 
      the latency of paw withdrawal from a thermal stimulus only on the ipsilateral 
      side. This thermal hyperalgesia was abolished by repeated intrathecal 
      pretreatment with a specific antibody to brain-derived neurotrophic factor 
      (BDNF), but not neurotrophin-4, just before and after the nerve ligation. These 
      results provide direct evidence that BDNF within the spinal cord may contribute 
      to the development of thermal hyperalgesia caused by nerve injury in mice. We 
      previously reported that protein level of full-length TrkB, which contains the 
      cytoplasmic protein tyrosine kinase domain, were clearly increased on the 
      ipsilateral side of spinal cord membranes obtained from sciatic nerve-ligated 
      mice. In the present study, we further demonstrated that the increased in the 
      protein level of full-length TrkB is completely reversed by concomitant 
      intrathecal injection of BDNF antibody. Furthermore, thermal hyperalgesia induced 
      by nerve ligation was completely suppressed by repeated intrathecal injection of 
      a specific antibody to full-length TrkB and an inhibitor of the protein tyrosine 
      kinase activity for the neurotrophin receptor, K-252a. However, repeated 
      intrathecal injection of a specific antibody to truncated TrkB, which lacks the 
      cytoplasmic protein tyrosine kinase domain, failed to reverse thermal 
      hyperalgesia observed in nerve-ligated mice. These findings suggest the 
      possibility that the binding of BDNF to full-length TrkB and subsequent its 
      activation may play a critical role in the development of neuropathic pain-like 
      thermal hyperalgesia induced by nerve injury in mice.
CI  - Copyright 2002 Elsevier Science B.V.
FAU - Yajima, Yoshinori
AU  - Yajima Y
AD  - Department of Toxicology, Hoshi University School of Pharmacy and Pharmaceutical 
      Sciences, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan.
FAU - Narita, Minoru
AU  - Narita M
FAU - Narita, Michiko
AU  - Narita M
FAU - Matsumoto, Nozomi
AU  - Matsumoto N
FAU - Suzuki, Tsutomu
AU  - Suzuki T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*antagonists & inhibitors/*physiology
MH  - Hot Temperature/adverse effects
MH  - Hyperalgesia/drug therapy/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Pain Measurement/drug effects/methods
MH  - Receptor, trkB/*antagonists & inhibitors/*physiology
MH  - Sciatic Neuropathy/drug therapy/*metabolism
MH  - Signal Transduction/drug effects/*physiology
MH  - Spinal Cord/drug effects/metabolism
EDAT- 2002/12/10 04:00
MHDA- 2003/03/28 05:00
CRDT- 2002/12/10 04:00
PHST- 2002/12/10 04:00 [pubmed]
PHST- 2003/03/28 05:00 [medline]
PHST- 2002/12/10 04:00 [entrez]
AID - S0006899302036661 [pii]
AID - 10.1016/s0006-8993(02)03666-1 [doi]
PST - ppublish
SO  - Brain Res. 2002 Dec 27;958(2):338-46. doi: 10.1016/s0006-8993(02)03666-1.