| Under many conditions spinal motoneurons produce plateau potentials, resulting in self-sustained firing and providing a mechanism for translating short-lasting synaptic inputs into long-lasting motor output. During the acute-stage of spinal cord injury (SCI), the endogenous ability to generate plateaus is lost; however, during the chronic-stage of SCI, plateau potentials reappear and have been implicated in the development of spasticity. The development of spasticity is an impediment to functional locomotor recovery after SCI. SCI results in changes in both motoneuron morphology and electrical behavior; however, it is not clear how these changes are related. In this dissertation, using a two-compartment model, previous modeling studies are extended to systematically investigate the mechanisms underlying the generation of plateau potentials in motoneurons, including the influences of specific ionic currents, the morphological characteristics of the soma and dendrite, and the interactions between persistent inward currents and synaptic input. Model results predict that the morphological changes commonly associated with chronic-stage SCI, such as increase in soma size and decrease in dendritic arbor cause a decrease in self-sustained firing. This suggests that increases in self-sustained firing observed during chronic-stage SCI occur due to changes in membrane conductances and changes in synaptic activity, particularly, changes in the strength and timing of inhibition. The two-compartment motoneuron model is extended to more biologically realistic multi-compartment equivalent cable models to study self-sustained firing in different motor unit types. The multi-compartment models are used to study the effects of dendritic geometry and spatial distributions of the ionic channels on self-sustained firing. |
