Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons

The withdrawal of synaptic inputs from the somata and proximal dendrites of spinal motoneurons following peripheral nerve injury could contribute to poor functional recovery. Decreased availability of neurotrophins to afferent terminals on axotomized motoneurons has been implicated as one cause of t...

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Main Authors: Joey Krakowiak, Caiyue Liu, Chandana Papudesu, P. Jillian Ward, Jennifer C. Wilhelm, Arthur W. English
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2015/392591
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author Joey Krakowiak
Caiyue Liu
Chandana Papudesu
P. Jillian Ward
Jennifer C. Wilhelm
Arthur W. English
author_facet Joey Krakowiak
Caiyue Liu
Chandana Papudesu
P. Jillian Ward
Jennifer C. Wilhelm
Arthur W. English
author_sort Joey Krakowiak
collection DOAJ
description The withdrawal of synaptic inputs from the somata and proximal dendrites of spinal motoneurons following peripheral nerve injury could contribute to poor functional recovery. Decreased availability of neurotrophins to afferent terminals on axotomized motoneurons has been implicated as one cause of the withdrawal. No reduction in contacts made by synaptic inputs immunoreactive to the vesicular glutamate transporter 1 and glutamic acid decarboxylase 67 is noted on axotomized motoneurons if modest treadmill exercise, which stimulates the production of neurotrophins by spinal motoneurons, is applied after nerve injury. In conditional, neuron-specific brain-derived neurotrophic factor (BDNF) knockout mice, a reduction in synaptic contacts onto motoneurons was noted in intact animals which was similar in magnitude to that observed after nerve transection in wild-type controls. No further reduction in coverage was found if nerves were cut in knockout mice. Two weeks of moderate daily treadmill exercise following nerve injury in these BDNF knockout mice did not affect synaptic inputs onto motoneurons. Treadmill exercise has a profound effect on synaptic inputs to motoneurons after peripheral nerve injury which requires BDNF production by those postsynaptic cells.
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series Neural Plasticity
spelling doaj-art-a1901c680bd945c2b261603814884d772025-02-03T05:58:19ZengWileyNeural Plasticity2090-59041687-54432015-01-01201510.1155/2015/392591392591Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized MotoneuronsJoey Krakowiak0Caiyue Liu1Chandana Papudesu2P. Jillian Ward3Jennifer C. Wilhelm4Arthur W. English5Department of Cell Biology, Emory University School of Medicine, 615 Michael Street, Room 405P, Atlanta, GA 30322, USADepartment of Plastic and Reconstructive Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, ChinaDepartment of Cell Biology, Emory University School of Medicine, 615 Michael Street, Room 405P, Atlanta, GA 30322, USADepartment of Cell Biology, Emory University School of Medicine, 615 Michael Street, Room 405P, Atlanta, GA 30322, USADepartment of Psychology, College of Charleston, 66 George Street, Charleston, SC 29424, USADepartment of Cell Biology, Emory University School of Medicine, 615 Michael Street, Room 405P, Atlanta, GA 30322, USAThe withdrawal of synaptic inputs from the somata and proximal dendrites of spinal motoneurons following peripheral nerve injury could contribute to poor functional recovery. Decreased availability of neurotrophins to afferent terminals on axotomized motoneurons has been implicated as one cause of the withdrawal. No reduction in contacts made by synaptic inputs immunoreactive to the vesicular glutamate transporter 1 and glutamic acid decarboxylase 67 is noted on axotomized motoneurons if modest treadmill exercise, which stimulates the production of neurotrophins by spinal motoneurons, is applied after nerve injury. In conditional, neuron-specific brain-derived neurotrophic factor (BDNF) knockout mice, a reduction in synaptic contacts onto motoneurons was noted in intact animals which was similar in magnitude to that observed after nerve transection in wild-type controls. No further reduction in coverage was found if nerves were cut in knockout mice. Two weeks of moderate daily treadmill exercise following nerve injury in these BDNF knockout mice did not affect synaptic inputs onto motoneurons. Treadmill exercise has a profound effect on synaptic inputs to motoneurons after peripheral nerve injury which requires BDNF production by those postsynaptic cells.http://dx.doi.org/10.1155/2015/392591
spellingShingle Joey Krakowiak
Caiyue Liu
Chandana Papudesu
P. Jillian Ward
Jennifer C. Wilhelm
Arthur W. English
Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
Neural Plasticity
title Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
title_full Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
title_fullStr Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
title_full_unstemmed Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
title_short Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons
title_sort neuronal bdnf signaling is necessary for the effects of treadmill exercise on synaptic stripping of axotomized motoneurons
url http://dx.doi.org/10.1155/2015/392591
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