PMID- 22492055
OWN - NLM
STAT- MEDLINE
DCOM- 20120529
LR  - 20211021
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 32
IP  - 14
DP  - 2012 Apr 4
TI  - Cooperative roles of BDNF expression in neurons and Schwann cells are modulated 
      by exercise to facilitate nerve regeneration.
PG  - 5002-9
LID - 10.1523/JNEUROSCI.1411-11.2012 [doi]
AB  - After peripheral nerve injury, neurotrophins play a key role in the regeneration 
      of damaged axons that can be augmented by exercise, although the distinct roles 
      played by neurons and Schwann cells are unclear. In this study, we evaluated the 
      requirement for the neurotrophin, brain-derived neurotrophic factor (BDNF), in 
      neurons and Schwann cells for the regeneration of peripheral axons after injury. 
      Common fibular or tibial nerves in thy-1-YFP-H mice were cut bilaterally and 
      repaired using a graft of the same nerve from transgenic mice lacking BDNF in 
      Schwann cells (BDNF(-/-)) or wild-type mice (WT). Two weeks postrepair, axonal 
      regeneration into BDNF(-/-) grafts was markedly less than WT grafts, emphasizing 
      the importance of Schwann cell BDNF. Nerve regeneration was enhanced by treadmill 
      training posttransection, regardless of the BDNF content of the nerve graft. We 
      further tested the hypothesis that training-induced increases in BDNF in neurons 
      allow regenerating axons to overcome a lack of BDNF expression in cells in the 
      pathway through which they regenerate. Nerves in mice lacking BDNF in YFP(+) 
      neurons (SLICK) were cut and repaired with BDNF(-/-) and WT nerves. SLICK axons 
      lacking BDNF did not regenerate into grafts lacking Schwann cell BDNF. Treadmill 
      training could not rescue the regeneration into BDNF(-/-) grafts if the neurons 
      also lacked BDNF. Both Schwann cell- and neuron-derived BDNF are thus important 
      for axon regeneration in cut peripheral nerves.
FAU - Wilhelm, Jennifer C
AU  - Wilhelm JC
AD  - Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 
      30322, USA. jennwilhelm@hotmail.com
FAU - Xu, Mei
AU  - Xu M
FAU - Cucoranu, Delia
AU  - Cucoranu D
FAU - Chmielewski, Sarah
AU  - Chmielewski S
FAU - Holmes, Tiffany
AU  - Holmes T
FAU - Lau, Kelly Shukkwan
AU  - Lau KS
FAU - Bassell, Gary J
AU  - Bassell GJ
FAU - English, Arthur W
AU  - English AW
LA  - eng
GR  - K12 GM000680-05/GM/NIGMS NIH HHS/United States
GR  - R01 HD055835-03/HD/NICHD NIH HHS/United States
GR  - NS057190/NS/NINDS NIH HHS/United States
GR  - R01 NS057190/NS/NINDS NIH HHS/United States
GR  - R01 NS057190-06A1/NS/NINDS NIH HHS/United States
GR  - HD055835/HD/NICHD NIH HHS/United States
GR  - K12 GM000680/GM/NIGMS NIH HHS/United States
GR  - R01 HD055835/HD/NICHD NIH HHS/United States
GR  - K12GM000680/GM/NIGMS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Axons/physiology
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis/physiology
MH  - Female
MH  - Gene Expression Regulation
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Nerve Regeneration/*physiology
MH  - Neurons/*metabolism
MH  - *Physical Conditioning, Animal/methods
MH  - Schwann Cells/*metabolism
MH  - Tibial Nerve/injuries/*physiology
PMC - PMC3382119
MID - NIHMS368798
EDAT- 2012/04/12 06:00
MHDA- 2012/05/30 06:00
PMCR- 2012/10/04
CRDT- 2012/04/12 06:00
PHST- 2012/04/12 06:00 [entrez]
PHST- 2012/04/12 06:00 [pubmed]
PHST- 2012/05/30 06:00 [medline]
PHST- 2012/10/04 00:00 [pmc-release]
AID - 32/14/5002 [pii]
AID - 3768329 [pii]
AID - 10.1523/JNEUROSCI.1411-11.2012 [doi]
PST - ppublish
SO  - J Neurosci. 2012 Apr 4;32(14):5002-9. doi: 10.1523/JNEUROSCI.1411-11.2012.