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Abstract
Spinal Cord Injury is a debilitating condition that has severe repercussions for individuals living with it. It involves multiple processes that are known to lead to cell death and a disruption of motor and sensory pathways. Little is known, however, about the health of the motor neurons that lie caudal to the injury and are deprived of supraspinal input. Knowledge about the viability of these cells is vital to the development of therapy that seeks to remediate the functionality that is lost as a result of injury. With this in view, this thesis sought to determine the morphological changes within motor neurons caudal to a transection of the Rubrospinal Tract (RST) in the rodent. It has previously been noted that disruptions to the RST result in deficits to skilled reaching and locomotion. The relationship between the hindlimb musculature in the mouse and the rat and the corresponding motor neurons that innervate these muscles were first characterised through injections of neuro-tracers along the entire span of the motor end plate (MEP) region of each muscle. Targeting the entire span of each MEP zone resulted in labelled motor neurons that extended in columns spanning more spinal segments than has been established in prior literature. Using the resultant innervation maps, the motor neurons that innervate Biceps Femoris and Vastus Medialis (muscles involved in locomotion) were selected to undergo stereological analysis to assess for morphological changes that occur as a result of the RST transection. The motor neuron column that innervates Pronator Teres was also included to assess for morphological changes. Analysis revealed no significant loss of neurons in the populations of small, medium and large motor neurons at both cervical and lumbar levels of the spinal cord between 1 to 14 days post-injury, on both sides of the spinal cord- ipsilateral and contralateral to the transection. This reveals that despite disruption of the motor circuitry that controls execution of fine motor movements and locomotion in the rodent, the motor neurons that have lost their supraspinal input remain viable and available for the application of therapeutic interventions that seek to remediate the lost functionality.