Repeated electrical nerve stimulation alterrs spinal motoneurons
What is it about?
Peripheral nerve injury is the most common type of nerve trauma, and behavioral recovery is protracted and typically poor. Neurotherapeutic approaches to injury have primarily focused on enhancing axonal regeneration, and both electrical stimulation and treatment with androgens have been demonstrated to improve regeneration rate and functional recovery. To date, very little work has been done to examine the effects of these treatments on motoneuron morphology after injury. We examined this question in rats who received a crush injury to the sciatic nerve. Following injury, some animals received either (1) no further treatment, (2) electrical nerve stimulation immediately after injury, (3) treatment with androgens, or (4) electrical nerve stimulation immediately after injury as well as androgen treatment. All of these groups of injured animals also received bi-weekly electromyography (EMG) testing. Additional groups of intact untreated animals as well as a group of injured animals who received no further treatment or EMG testing were also included. Eight weeks after injury, the morphology of motoneurons contributing to the sciatic nerve was assessed. We found that after nerve crush and electrical nerve stimulation and/or treatment with androgens, sciatic motoneurons underwent marked dendritic hypertrophy. Surprisingly, this dendritic hypertrophy occurred in all animals receiving repeated electrical nerve stimulation through bi-weekly EMG testing, regardless of treatment. When the repeated electrical nerve stimulation was eliminated, the dendritic arbor hypertrophy was absent, and motoneuron morphology did not differ from that of intact untreated animals. The ability of repeated electrical nerve stimulation to so dramatically affect central plasticity following a peripheral nerve injury was unexpected. It was also unexpected that electrical stimulation and/or androgen treatment, two neurotherapeutic approaches with demonstrated molecular/behavioral changes consistent with peripheral improvements in axonal repair and target reconnection, do not appear to impact central plasticity in a similar manner. The significance of repeated electrical nerve stimulation and resulting central plasticity reorganization remains to be determined. Are there negative and/or positive ramifications associated with functional recovery that ultimately impact activities of daily living for the neurologically impaired individual? Further morphological and behavioral studies will be necessary to address these questions in follow-up to the results reported in our work.