Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise

• Type of Material: Article
• Authors: Tessa Gordon, The Hospital for Sick Children; Arthur English, Emory University
• Language: English
• Date: 2016-02-01
• Publisher: Wiley: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
• Final Published Version (URL): http://dx.doi.org/10.1111/ejn.13005
• Title of Journal or Parent Work: European Journal of Neuroscience
• ISSN: 0953-816X
• Volume: 43
• Issue: 3
• Start Page: 336
• End Page: 350
• Keywords: Science & Technology; WALLERIAN DEGENERATION; SCHWANN-CELLS; exercise and nerve regeneration; peripheral nerve regeneration; CENTRAL SYNAPTIC DISCONNECTION; MOTOR AXONS; RAT FACIAL-NERVE; SCIATIC-NERVE; NEUROTROPHIC FACTOR EXPRESSION; CRUSH INJURY; electrical stimulation; AXON REGENERATION; Life Sciences & Biomedicine; exercise or electrical stimulation; Neurosciences; nerve stimulation; Neurosciences & Neurology; ENHANCES FUNCTIONAL RECOVERY
• Research Categories: Biology, Physiology; Biology, Cell; Biology, Neuroscience

Abstract

Enhancing the regeneration of axons is often considered to be a therapeutic target for improving functional recovery after peripheral nerve injury. In this review, the evidence for the efficacy of electrical stimulation (ES), daily exercise and their combination in promoting nerve regeneration after peripheral nerve injuries in both animal models and in human patients is explored. The rationale, effectiveness and molecular basis of ES and exercise in accelerating axon outgrowth are reviewed. In comparing the effects of ES and exercise in enhancing axon regeneration, increased neural activity, neurotrophins and androgens are considered to be common requirements. Similarly, there are sex-specific requirements for exercise to enhance axon regeneration in the periphery and for sustaining synaptic inputs onto injured motoneurons. ES promotes nerve regeneration after delayed nerve repair in humans and rats. The effectiveness of exercise is less clear. Although ES, but not exercise, results in a significant misdirection of regenerating motor axons to reinnervate different muscle targets, the loss of neuromuscular specificity encountered has only a very small impact on resulting functional recovery. Both ES and exercise are promising experimental treatments for peripheral nerve injury that seem to be ready to be translated to clinical use.