title: Transection of preganglionic axons leads to CNS neuronal plasticity followed by survival and target reinnervation.
abstract: 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.
authors.affiliation: 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.
authors.forename: Aminata P
authors.initials: AP
authors.lastname: Coulibaly
authors.forename: Sean M
authors.initials: SM
authors.lastname: Gannon
authors.forename: Kiel
authors.initials: K
authors.lastname: Hawk
authors.forename: Brian F
authors.initials: BF
authors.lastname: Walsh
authors.forename: Lori G
authors.initials: LG
authors.lastname: Isaacson
mesh_terms: D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000502:physiology*; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure*; D019771:Axotomy; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000096:biosynthesis; D005260:Female; D005455:Fluorescent Antibody Technique; D020287:In Situ Nick-End Labeling; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020813:Receptor, trkB / Q000096:biosynthesis; D013116:Spinal Cord / Q000378:metabolism*; D017783:Superior Cervical Ganglion / Q000502:physiology
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D020813:Receptor, trkB
keywords: Brain derived neurotrophic factor (BDNF); CNS response to peripheral injury; Full length TrkB (TrkB.FL); Intermediolateral cell column (IML); Neurotrophin regulation; Retrograde signaling following injury; Truncated TrkB (TrkB.T1)
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