PMID- 23891533
OWN - NLM
STAT- MEDLINE
DCOM- 20140806
LR  - 20211021
IS  - 1872-7484 (Electronic)
IS  - 1566-0702 (Print)
IS  - 1566-0702 (Linking)
VI  - 179
IP  - 1-2
DP  - 2013 Dec
TI  - Transection of preganglionic axons leads to CNS neuronal plasticity followed by 
      survival and target reinnervation.
PG  - 49-59
LID - S1566-0702(13)00603-6 [pii]
LID - 10.1016/j.autneu.2013.07.002 [doi]
AB  - The goals of the present study were to investigate the changes in sympathetic 
      preganglionic neurons following transection of distal axons in the cervical 
      sympathetic trunk (CST) that innervate the superior cervical ganglion (SCG) and 
      to assess changes in the protein expression of brain derived neurotrophic factor 
      (BDNF) and its receptor TrkB in the thoracic spinal cord. At 1 week, a 
      significant decrease in soma volume and reduced soma expression of choline 
      acetyltransferase (ChAT) in the intermediolateral cell column (IML) of T1 spinal 
      cord were observed, with both ChAT-ir and non-immunoreactive neurons expressing 
      the injury marker activating transcription factor 3. These changes were 
      transient, and at later time points, ChAT expression and soma volume returned to 
      control values and the number of ATF3 neurons declined. No evidence for cell loss 
      or neuronal apoptosis was detected at any time point. Protein levels of BDNF 
      and/or full length TrkB in the spinal cord were increased throughout the survival 
      period. In the SCG, both ChAT-ir axons and ChAT protein remained decreased at 16 
      weeks, but were increased compared to the 10 week time point. These results 
      suggest that though IML neurons show reduced ChAT expression and cell volume at 1 
      week following CST transection, at later time points, the neurons recovered and 
      exhibited no significant signs of neurodegeneration. The alterations in BDNF 
      and/or TrkB may have contributed to the survival of the IML neurons and the 
      recovery of ChAT expression, as well as to the reinnervation of the SCG.
CI  - (c) 2013.
FAU - Coulibaly, Aminata P
AU  - Coulibaly AP
AD  - Center for Neuroscience and Behavior, Miami University, Oxford, OH 45056, United 
      States; Graduate Program in Cell, Molecular, and Structural Biology, Miami 
      University, Oxford, OH 45056, United States.
FAU - Gannon, Sean M
AU  - Gannon SM
FAU - Hawk, Kiel
AU  - Hawk K
FAU - Walsh, Brian F
AU  - Walsh BF
FAU - Isaacson, Lori G
AU  - Isaacson LG
LA  - eng
GR  - R15 NS051206/NS/NINDS NIH HHS/United States
GR  - NS051206/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20130724
PL  - Netherlands
TA  - Auton Neurosci
JT  - Autonomic neuroscience : basic & clinical
JID - 100909359
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Autonomic Fibers, Preganglionic/*physiology
MH  - Axons/*physiology/*ultrastructure
MH  - Axotomy
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/biosynthesis
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - In Situ Nick-End Labeling
MH  - Nerve Regeneration/*physiology
MH  - *Neuronal Plasticity/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/biosynthesis
MH  - Spinal Cord/*metabolism
MH  - Superior Cervical Ganglion/physiology
PMC - PMC3843981
MID - NIHMS505143
OTO - NOTNLM
OT  - Brain derived neurotrophic factor (BDNF)
OT  - CNS response to peripheral injury
OT  - Full length TrkB (TrkB.FL)
OT  - Intermediolateral cell column (IML)
OT  - Neurotrophin regulation
OT  - Retrograde signaling following injury
OT  - Truncated TrkB (TrkB.T1)
EDAT- 2013/07/31 06:00
MHDA- 2014/08/07 06:00
PMCR- 2014/12/01
CRDT- 2013/07/30 06:00
PHST- 2013/03/27 00:00 [received]
PHST- 2013/06/17 00:00 [revised]
PHST- 2013/07/04 00:00 [accepted]
PHST- 2013/07/30 06:00 [entrez]
PHST- 2013/07/31 06:00 [pubmed]
PHST- 2014/08/07 06:00 [medline]
PHST- 2014/12/01 00:00 [pmc-release]
AID - S1566-0702(13)00603-6 [pii]
AID - 10.1016/j.autneu.2013.07.002 [doi]
PST - ppublish
SO  - Auton Neurosci. 2013 Dec;179(1-2):49-59. doi: 10.1016/j.autneu.2013.07.002. Epub 
      2013 Jul 24.