Abstract

Ultrasound stimulation (US) is reported to be a safe and useful technology for improving injured nerve regeneration. However, the intracellular mechanisms underlying its stimulatory effects are only partially understood. Mammalian target of rapamycin (mTOR) signaling is involved in neuronal survival and axonal outgrowth. In this study, we investigated the effect of US on regeneration of injured dorsal root ganglion (DRG) neurons and activation of the mTOR pathway. We showed that US significantly increased neurite regeneration and enhanced mTOR activation. Moreover, the expression of growth-associated protein-43 (GAP-43), a crucial factor for axonal outgrowth and regeneration in neurons, was significantly increased by US. These data suggest that US-induced neurite regeneration is mediated by upregulation of mTOR activity, which promotes the regeneration of injured DRG neurons.

Highlights

  • Nerve injury is commonly caused by accidental trauma and results in disconnection and disruption of axonal pathways, leading to permanent physiological impairments, such as paralysis and loss of sensation [1,2]

  • To analyze the effect of ultrasound stimulation (US) on neurite regeneration, dorsal root ganglion (DRG) explant neurites were grown to a length that allowed axotomy, and morphological changes and neurite regeneration were observed

  • DRG explants with neurites that were three times longer than the diameter of the DRG explants after five days of culture were used in this experiment

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Summary

Introduction

Nerve injury is commonly caused by accidental trauma and results in disconnection and disruption of axonal pathways, leading to permanent physiological impairments, such as paralysis and loss of sensation [1,2]. Whereas the central nervous system (CNS) has a limited ability for repair and regeneration, resulting in permanent damage after injury, axons in the peripheral nervous system (PNS) can spontaneously regenerate following injury [3,4]. The functional recovery of peripheral nerves following clinical injury is highly limited and unsatisfactory. Delayed axonal regeneration can result in functional impairments despite nerve continuity. Increasing the speed and efficacy of axonal regeneration is important for achieving successful regeneration after peripheral nerve injury

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