PMID- 17183451
OWN - NLM
STAT- MEDLINE
DCOM- 20070315
LR  - 20161021
IS  - 1641-4640 (Print)
IS  - 1509-572X (Linking)
VI  - 44
IP  - 4
DP  - 2006
TI  - TrkB deficiency increases survival and regeneration of spinal motoneurons after 
      axotomy in mice.
PG  - 251-6
AB  - Persisting motor function deficit after peripheral nerve injury often results 
      from axotomized motoneuron death. Brain-derived neurotrophic factor (BDNF) and 
      its receptor, trkB, are known to promote peripheral nerve regeneration. However, 
      the requirement of BDNF and trkB for adult motoneuron survival after peripheral 
      nerve injury is not established. We studied the number of surviving and 
      regenerating motoneurons after sciatic nerve transection in wild-type and 
      heterozygous trkB-deficient mice. The nerve was either left cut or immediately 
      sewed up or the gap injury model was performed. The gap was provided with an 
      autologous or cross (obtained from other genetic group) graft. Sixteen weeks 
      after surgery, the animals were sacrificed and histological evaluations were 
      performed. In order to study the number of regenerating motoneurons, 
      immunofluorescent tracer was applied to the distal stump of the operated nerve. 
      We found that in wild type mice, the decrease in motoneurons after nerve 
      transection was markedly higher than in trkB-deficient animals, regardless of the 
      operation procedure. Nerve transection resulted in the highest decrease in 
      motoneuron number in wild type mice. This decrease was lower if the nerve was 
      re-joined using a cross-graft obtained from a trkB-deficient animal. 
      Interestingly, in trkB-deficient animals, the decrease in motoneuron count did 
      not depend on type of operation and was similar after nerve transection, 
      re-joining or grafting. The number of regenerating motoneurons after nerve 
      transection and re-joining in wild type animals was lower than in trkB-deficient 
      mice. The number of regenerating motoneurons after nerve grafting did not differ 
      between groups. These results provide further evidence for the role of trkB 
      receptor in spinal motoneuron survival and regeneration.
FAU - Kotulska, Katarzyna
AU  - Kotulska K
AD  - Department of Neurology, The Children's Memorial Health Institute, al. Dzieci 
      Polskich 20, 04-730 Warsaw, Poland. k.kotulska@czd.pl
FAU - Larysz-Brysz, Magdalena
AU  - Larysz-Brysz M
FAU - Marcol, Wieslaw
AU  - Marcol W
FAU - Malinowska, Izabela
AU  - Malinowska I
FAU - Matuszek, Iwona
AU  - Matuszek I
FAU - Grajkowska, Wieslawa
AU  - Grajkowska W
FAU - Lewin-Kowalik, Joanna
AU  - Lewin-Kowalik J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - Folia Neuropathol
JT  - Folia neuropathologica
JID - 9437431
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - *Axotomy
MH  - Cell Survival
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Motor Neurons/*pathology
MH  - *Nerve Regeneration
MH  - Receptor, trkB/*deficiency
MH  - Spinal Cord/metabolism/*pathology/*physiopathology
EDAT- 2006/12/22 09:00
MHDA- 2007/03/16 09:00
CRDT- 2006/12/22 09:00
PHST- 2006/12/22 09:00 [pubmed]
PHST- 2007/03/16 09:00 [medline]
PHST- 2006/12/22 09:00 [entrez]
AID - 7178 [pii]
PST - ppublish
SO  - Folia Neuropathol. 2006;44(4):251-6.