scholarly journals Exercise, Neurotrophins, and Axon Regeneration in the PNS

Physiology ◽  
2014 ◽  
Vol 29 (6) ◽  
pp. 437-445 ◽  
Author(s):  
Arthur W. English ◽  
Jennifer C. Wilhelm ◽  
Patricia J. Ward
Keyword(s):  
Electrical Stimulation ◽  
Androgen Receptor ◽  
Peripheral Nerve ◽  
Neuronal Activity ◽  
Axon Regeneration ◽  
Sex Steroid ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries ◽  
Cellular Mechanisms ◽  
Androgen Receptor Signaling

Electrical stimulation and exercise are treatments to enhance recovery from peripheral nerve injuries. Brain-derived neurotrophic factor and androgen receptor signaling are requirements for the effectiveness of these treatments. Increased neuronal activity is adequate to promote regeneration in injured nerves, but the dosing of activity and its relationship to neurotrophins and sex steroid hormones is less clear. Translation of these therapies will require principles associated with their cellular mechanisms.

scholarly journals Electrical Stimulation to Promote Peripheral Nerve Regeneration

2015 ◽  
Vol 30 (5) ◽  
pp. 490-496 ◽  
Author(s):  
Michael P. Willand ◽  
May-Anh Nguyen ◽  
Gregory H. Borschel ◽  
Tessa Gordon
Keyword(s):  
Electrical Stimulation ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Functional Recovery ◽  
Axonal Regeneration ◽  
Surgical Repair ◽  
Primary Repair ◽  
Low Frequency ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries

Peripheral nerve injury afflicts individuals from all walks of life. Despite the peripheral nervous system’s intrinsic ability to regenerate, many patients experience incomplete functional recovery. Surgical repair aims to expedite this recovery process in the most thorough manner possible. However, full recovery is still rarely seen especially when nerve injury is compounded with polytrauma where surgical repair is delayed. Pharmaceutical strategies supplementary to nerve microsurgery have been investigated but surgery remains the only viable option. Brief low-frequency electrical stimulation of the proximal nerve stump after primary repair has been widely investigated. This article aims to review the currently known biological basis for the regenerative effects of acute brief low-frequency electrical stimulation on axonal regeneration and outline the recent clinical applications of the electrical stimulation protocol to demonstrate the significant translational potential of this modality for repairing peripheral nerve injuries. The review concludes with a discussion of emerging new advancements in this exciting area of research. The current literature indicates the imminent clinical applicability of acute brief low-frequency electrical stimulation after surgical repair to effectively promote axonal regeneration as the stimulation has yielded promising evidence to maximize functional recovery in diverse types of peripheral nerve injuries.

Peripheral Nerve Injuries of the Shoulder in the Athlete

1990 ◽  
Vol 9 (2) ◽  
pp. 331-342 ◽  
Author(s):  
Francis X. Mendoza ◽  
Kenneth Main
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries

scholarly journals Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. I. Loss of VGLUT1/IA synapses on motoneurons

2011 ◽  
Vol 106 (5) ◽  
pp. 2450-2470 ◽  
Author(s):  
Francisco J. Alvarez ◽  
Haley E. Titus-Mitchell ◽  
Katie L. Bullinger ◽  
Michal Kraszpulski ◽  
Paul Nardelli ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Cell Body ◽  
Peripheral Nerve Injury ◽  
Motor Coordination ◽  
Electrophysiological Study ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries ◽  
Ia Afferent ◽  
Axon Collaterals

Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75–95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral projections, we studied the central trajectories and synaptic varicosities of axon collaterals from control and regenerated afferents with IA-like responses to stretch that were intracellularly filled with neurobiotin. VGLUT1 was present in all synaptic varicosities, identified with the synaptic marker SV2, of control and regenerated afferents. However, regenerated afferents lacked axon collaterals and synapses in lamina IX. In conjunction with the companion electrophysiological study [Bullinger KL, Nardelli P, Pinter MJ, Alvarez FJ, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01097.2010], we conclude that peripheral nerve injuries cause a permanent retraction of IA afferent synaptic varicosities from lamina IX and disconnection with motoneurons that is not recovered after peripheral regeneration and reinnervation of muscle by sensory and motor axons.

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