During development and throughout life, descending activity from the brain shapes spinal cord reflexes to support effective motor function. When injury or disease impairs this long-term supraspinal control, the reflex patterns are distorted and spasticity and other disabling problems appear. The mechanisms of supraspinal control of spinal cord plasticity are not well understood. Better understanding would elucidate the mechanisms of acquisition of motor skills, and could lead to novel methods for inducing, guiding, and assessing recovery of function after spinal cord injury. Operant conditioning of the spinal stretch reflex (or tendon jerk) or its electrical analog, the H-reflex, is a simple model for exploring long-term supraspinal control of spinal cord plasticity. In response to an operant conditioning protocol, monkeys, humans, and rats can gradually increase or decrease the SSR or the H-reflex. The learning changes the spinal cord, since evidence of it remains even after all supraspinal control is removed. This lab is using H-reflex conditioning in the rat to explore supraspinal control of this spinal cord plasticity. The central goal of this project is to determine which spinal cord pathways and which supraspinal areas are responsible for acquisition and maintenance of the spinal cord plasticity caused by H-reflex conditioning. The central hypotheses, supported by recent studies and preliminary data, are: (1) that the main corticospinal tract is essential for acquisition and maintenance of H-reflex conditioning and that the rubrospinal tract and other major descending and ascending pathways are not essential; and (2) that sensorimotor cortex, cerebellum, and cerebellar-cortical connections are essential for acquisition and maintenance of H-reflex conditioning. These hypotheses will be tested by studying the effects of lesions of pyramidal tract, rubrospinal tract, contralateral and ipsilateral sensorimotor cortices, cerebellar nuclei and other areas on acquisition and maintenance of H-reflex up-conditioning and down-conditioning. The results should lead to new understanding of how the brain shapes spinal cord reflexes so that they support effective motor function. They could also promote development of a promising new method for inducing and guiding spinal cord plasticity that could, in combination with other new therapeutic methods (such as those that promote regeneration), help to maximize restoration of function after spinal cord injury.
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