scholarly journals Delaying the onset of treadmill exercise following peripheral nerve injury has different effects on axon regeneration and motoneuron synaptic plasticity

2015 ◽  
Vol 113 (7) ◽  
pp. 2390-2399 ◽  
Author(s):  
Jaclyn Brandt ◽  
Jonathan T. Evans ◽  
Taylor Mildenhall ◽  
Amanda Mulligan ◽  
Aimee Konieczny ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Axon Regeneration ◽  
Treadmill Exercise ◽  
Glutamate Transporter ◽  
Interval Training ◽  
Therapeutic Window ◽  
Acid Decarboxylase ◽  
Glutamate Transporter 1

Transection of a peripheral nerve results in withdrawal of synapses from motoneurons. Some of the withdrawn synapses are restored spontaneously, but those containing the vesicular glutamate transporter 1 (VGLUT1), and arising mainly from primary afferent neurons, are withdrawn permanently. If animals are exercised immediately after nerve injury, regeneration of the damaged axons is enhanced and no withdrawal of synapses from injured motoneurons can be detected. We investigated whether delaying the onset of exercise until after synapse withdrawal had occurred would yield similar results. In Lewis rats, the right sciatic nerve was cut and repaired. Reinnervation of the soleus muscle was monitored until a direct muscle (M) response was observed to stimulation of the tibial nerve. At that time, rats began 2 wk of daily treadmill exercise using an interval training protocol. Both M responses and electrically-evoked H reflexes were monitored weekly for an additional seven wk. Contacts made by structures containing VGLUT1 or glutamic acid decarboxylase (GAD67) with motoneurons were studied from confocal images of retrogradely labeled cells. Timing of full muscle reinnervation was similar in both delayed and immediately exercised rats. H reflex amplitude in delayed exercised rats was only half that found in immediately exercised animals. Unlike immediately exercised animals, motoneuron contacts containing VGLUT1 in delayed exercised rats were reduced significantly, relative to intact rats. The therapeutic window for application of exercise as a treatment to promote restoration of synaptic inputs onto motoneurons following peripheral nerve injury is different from that for promoting axon regeneration in the periphery.

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

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Joey Krakowiak ◽  
Caiyue Liu ◽  
Chandana Papudesu ◽  
P. Jillian Ward ◽  
Jennifer C. Wilhelm ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Knockout Mice ◽  
Peripheral Nerve Injury ◽  
Treadmill Exercise ◽  
Glutamate Transporter ◽  
Acid Decarboxylase ◽  
Spinal Motoneurons ◽  
Synaptic Inputs ◽  
Glutamate Transporter 1

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.

scholarly journals Bioluminescent Optogenetics: A Novel Experimental Therapy to Promote Axon Regeneration after Peripheral Nerve Injury

2021 ◽  
Vol 22 (13) ◽  
pp. 7217
Author(s):  
Arthur W. English ◽  
Ken Berglund ◽  
Dario Carrasco ◽  
Katharina Goebel ◽  
Robert E. Gross ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Viral Vectors ◽  
Axon Regeneration ◽  
Intraperitoneal Administration ◽  
Experimental Therapy ◽  
Promising Therapeutic Approach ◽  
Compound Muscle Action Potentials

Functional recovery after peripheral nerve injury (PNI) is poor, mainly due to the slow and incomplete regeneration of injured axons. Experimental therapies that increase the excitability of the injured axons have proven remarkably successful in promoting regeneration, but their clinical applicability has been limited. Bioluminescent optogenetics (BL-OG) uses luminopsins, fusion proteins of light-generating luciferase and light-sensing ion channels that could be used to increase neuronal excitability if exposed to a suitable substrate. Excitatory luminopsins were expressed in motoneurons of transgenic mice and in wildtype mice transduced with adeno-associated viral vectors. Intraperitoneal administration of coelenterazine (CTZ), a known luciferase substrate, generated intense bioluminescence in peripheral axons. This bioluminescence increased motoneuron excitability. A single administration of CTZ immediately after sciatic nerve transection and repair markedly enhanced motor axon regeneration. Compound muscle action potentials were 3–4 times larger than controls by 4 weeks after injury. The results observed with transgenic mice were comparable to those of mice in which the luminopsin was expressed using viral vectors. Significantly more motoneurons had successfully reinnervated muscle targets four weeks after nerve injury in BL-OG treated mice than in controls. Bioluminescent optogenetics is a promising therapeutic approach to enhancing axon regeneration after PNI.

Comparing axon regeneration in male and female mice after peripheral nerve injury

2021 ◽  
Author(s):  
Eun‐Hae Jang ◽  
Yun‐Hee Bae ◽  
Eun Mo Yang ◽  
Yunho Gim ◽  
Hyun‐Jun Suh ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Axon Regeneration ◽  
Male And Female ◽  
Female Mice

scholarly journals Intracellular phospholipase A2 group IVA and group VIA play important roles in Wallerian degeneration and axon regeneration after peripheral nerve injury

Brain ◽  
2008 ◽  
Vol 131 (10) ◽  
pp. 2620-2631 ◽  
Author(s):  
Rubèn López-Vales ◽  
Xavier Navarro ◽  
Takao Shimizu ◽  
Constantinos Baskakis ◽  
George Kokotos ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Phospholipase A2 ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Wallerian Degeneration ◽  
Axon Regeneration ◽  
Group Iva

Endogenous modulation of TrkB signaling by treadmill exercise after peripheral nerve injury

Neuroscience ◽  
2017 ◽  
Vol 340 ◽  
pp. 188-200 ◽  
Author(s):  
Ariadna Arbat-Plana ◽  
Stefano Cobianchi ◽  
Mireia Herrando-Grabulosa ◽  
Xavier Navarro ◽  
Esther Udina
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Treadmill Exercise

scholarly journals Bioinformatics analysis of long non-coding RNAs involved in nerve regeneration following sciatic nerve injury

2020 ◽  
Vol 16 ◽  
pp. 174480692097191
Author(s):  
Yuanyuan Jia ◽  
Ming Zhang ◽  
Pei Li ◽  
Wenbo Tang ◽  
Yao Liu ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Axon Regeneration ◽  
Sciatic Nerve Injury ◽  
Sciatic Nerve Crush ◽  
Non Coding Rnas

Little is known about the role of epigenetic modification in axon regeneration following peripheral nerve injury. The purpose of the present study was to investigate the role of long non-coding RNAs (lncRNAs) in the regulation of axon regeneration. We used bioinformatics to perform microarray analysis and screened total 476 lncRNAs and 129 microRNAs (miRNAs) of differentially expressed genes after sciatic nerve injury in mice. lncRNA-GM4208 and lncRNA-GM30085 were examined, and the changes in lncRNA expression in the L4–L6 dorsal root ganglia (DRG) following sciatic nerve crush injury were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression of lncRNAs in the DRG changed, indicating that they might be related to nerve regeneration in the DRG following peripheral nerve injury.

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