PMID- 11223157
OWN - NLM
STAT- MEDLINE
DCOM- 20010809
LR  - 20190826
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 87
IP  - 1
DP  - 2001 Feb 19
TI  - Axotomy alters neurotrophin and neurotrophin receptor mRNAs in the vagus nerve 
      and nodose ganglion of the rat.
PG  - 31-41
AB  - Neurotrophins and neurotrophin receptors play an important role in survival and 
      growth of injured peripheral nerves. To study the injury-mediated neurotrophic 
      response in autonomic nerves, we investigated changes in mRNA expression of 
      neurotrophins and their receptors in the transected vagus nerve and nodose 
      ganglion. Studies using in situ hybridization histochemistry showed that axotomy 
      of the cervical vagus nerve resulted in increased expression of mRNAs for nerve 
      growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 
      (NT-3), and for TrkA, TrkB, and TrkC receptors in non-neuronal cells at both the 
      proximal and distal segments of the transected cervical vagus nerve. Moreover, 
      NGF protein was increased in the distal end, and NT-3 protein was increased in 
      both the proximal and the distal ends of the transected nerve 3 days after 
      axotomy. No change of p75(NTR) mRNA was detected in the transected vagus nerve. 
      The induction of each neurotrophin and Trk receptor mRNA was apparent within 1 
      day after the axotomy and was sustained at least 14 days. By 45 days after the 
      axotomy, a time when axonal reconnection with target tissue is made (integrity of 
      the nerve-target connection was confirmed by the retrograde transport of 
      FluoroGold from the stomach to vagal cell bodies), the levels of neurotrophin and 
      Trk mRNAs in the vagus nerve declined to pre-axotomy levels. TrkA, TrkC, and 
      p75(NTR) mRNA-containing vagal sensory neurons in the nodose ganglion were 
      reduced in number after cervical vagotomy. Neurotrophin-mRNA-containing neurons 
      were not found in the nodose ganglia from either intact or vagotomized rats. The 
      axotomy-induced up-regulation of neurotrophins and Trk receptors mainly in the 
      non-neuronal cells at or near the site of transection suggests that neurotrophins 
      are involved in the survival and regeneration process of the vagus nerve after 
      injury.
FAU - Lee, P
AU  - Lee P
AD  - Department of Pharmacology, Uniformed Services University of the Health Sciences, 
      4301 Jones Bridge Road, 20814, Bethesda, MD, USA.
FAU - Zhuo, H
AU  - Zhuo H
FAU - Helke, C J
AU  - Helke CJ
LA  - eng
GR  - NS20991/NS/NINDS NIH HHS/United States
GR  - NS38845/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neurotrophin 3)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (Receptor, trkC)
SB  - IM
MH  - Animals
MH  - Axotomy
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Gene Expression/physiology
MH  - Male
MH  - Nerve Regeneration/physiology
MH  - Neurotrophin 3/analysis/*genetics
MH  - Nodose Ganglion/chemistry/injuries/*physiology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Nerve Growth Factor/genetics
MH  - Receptor, trkA/genetics
MH  - Receptor, trkB/genetics
MH  - Receptor, trkC/genetics
MH  - Receptors, Nerve Growth Factor/analysis/*genetics
EDAT- 2001/02/27 10:00
MHDA- 2001/08/10 10:01
CRDT- 2001/02/27 10:00
PHST- 2001/02/27 10:00 [pubmed]
PHST- 2001/08/10 10:01 [medline]
PHST- 2001/02/27 10:00 [entrez]
AID - S0169328X00002771 [pii]
AID - 10.1016/s0169-328x(00)00277-1 [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 2001 Feb 19;87(1):31-41. doi: 
      10.1016/s0169-328x(00)00277-1.