Suppressing the excitability of spinal motoneurons by extracellularly applied electrical fields: insights from computer simulations.
The effect of extracellularly applied electrical fields on neuronal excitability and firing behavior is attributed to the interaction between neuronal morphology and the spatial distribution and level of differential polarization induced by the applied field in different elements of the neuron. The presence of voltage-gated ion channels that mediate persistent inward currents (PICs) on the dendrites of spinal motoneurons enhances the influence of electrical fields on the motoneuronal firing behavior. The goal of the present study was to investigate, with a realistic motoneuron computer model, the effects of extracellularly applied electrical fields on the excitability of spinal motoneurons with the aim of reducing the increased motoneuronal excitability after spinal cord injury (SCI). Our results suggest that electrical fields could suppress the excitability of motoneurons and reduce their firing rate significantly by modulating the magnitude of their dendritic PIC. This effect was achieved at different field directions, intensities, and polarities. The reduction in motoneuronal firing rate resulted from the reduction in the magnitude of the dendritic PIC reaching the soma by the effect of the applied electrical field. This reduction in PIC was attributed to the dendritic field-induced differential polarization and the nonlinear current-voltage relationship of the dendritic PIC-mediating channels. Because of the location of the motoneuronal somata and initial segment with respect to the dendrites, these structures were minimally polarized by the applied field compared with the extended dendrites. In conclusion, electrical fields could be used for suppressing the hyperexcitability of spinal motoneurons after SCI and reducing the level of spasticity.
Elbasiouny
Sherif M
SM
Department of Biomedical Engineering , Univ. of Alberta, Edmonton, AB, Canada T6G 2S2.
Mushahwar
Vivian K
VK
D000200:Action Potentials; D000818:Animals; D002415:Cats; D003198:Computer Simulation; D003712:Dendrites / Q000378:metabolism*; D004558:Electric Stimulation / Q000379:methods; D004599:Electric Stimulation Therapy / Q000379:methods; D005240:Feasibility Studies; D007473:Ion Channels / Q000378:metabolism*; D008959:Models, Neurological; D009046:Motor Neurons / Q000378:metabolism*; D009128:Muscle Spasticity / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D009431:Neural Conduction; D009433:Neural Inhibition; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D013127:Spinal Nerves / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors
D007473:Ion Channels