Modulation of H-reflex responses and frequency-dependent depression by repetitive spinal electromagnetic stimulation: From rats to humans and back to chronic spinal cord injured rats.

Abstract

The lack of propagation of signals through survived fibers is among the major reasons for functional loss after incomplete spinal cord injury (SCI). Our recent results of animal studies demonstrate that spinal electromagnetic stimulation (SEMS) can enhance transmission in damaged spinal cord, and this type of modulation depends on the function of NMDA receptors at the neuronal networks below the injury level. Here, our pilot human study revealed that administration of repetitive SEMS induced long‐lasting modulation of H‐responses in both healthy and participants with chronic SCI. In order to understand the mechanisms underlying these effects, we have used an animal model and examined effects of SEMS on H‐responses. Effects of SEMS on H‐responses, frequency‐dependent depression (FDD) of H‐reflex, and possible underlying mechanisms have been examined in both naïve and rats with SCI. Our results demonstrate that consistent with the effects of SEMS on H‐reflex seen in humans, repetitive SEMS induced similar modulation in excitability of peripheral nerve responses in both non‐injured and rats with SCI. Importantly, our results confirmed the reduced FDD of H‐reflex in SCI animals and revealed that SEMS was able to recover FDD in rats with chronic SCI. Using intraspinal injections of the NMDA receptor blocker MK‐801, we have identified NMDA receptors as an important contributor to these SEMS‐induced effects in rats with SCI. These results identify SEMS as a novel non‐invasive technique for modulation of neuro‐muscular circuits and, importantly, modulation of spinal networks after chronic SCI.