Electrical stimulation effects on PNS injury and repair are mediated by accelerating intracellular trafficking?

Abstract

Peripheral nerve injury and repair is a complex and dynamic process including the outgrowth of newborn axons, the selecting targeting of regenerating axons and their remyelination. The whole process is finely modulated and affected by various regeneration-associated factors and other molecules cooperating with them. The emphasis of current studies aims to improve nerve repair and functional recovery by coordinating the activity of each member involved in the teamwork of nerve regeneration. The neural cells are highly polarized, most of which develop various subcellular compartments including the cell body and processes, respectively participating in the consecutive synthesis and delivery of genes and proteins. Some RNAs synthesized at perikaryon are selectively transported to the distal end and translated into proteins locally. Some proteins choose the way to the distal part of the growing process and play biological functions there. Changes of the microenvironment could induce intracellular biosynthesis at the nucleus and processes thereby to impact the network between cells. Although the route of the specific trafficking of genes and proteins is only partly revealed, it is a feasible means to facilitate negotiation between the nucleus and the distal reaches in this way to assist nerve repair. Electrical stimulation as a convenient technique was applied extensively to clinical therapies on nervous diseases and proved to produce marked effects. But the underlying mechanism of electrical stimulation on nerve injury and repair is poorly understood. We speculate that electrical stimulation therapies take part in nerve degeneration and regeneration not only by stimulating the neural cells to synthesize regeneration-associated genes and proteins, but also by accelerating their transport and promote the localized genes translation at the lesion site.