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Prior studies have shown that exposure to uncontrollable stimulation can have a variety of adverse consequences on plasticity. For example, as little as 30 min of uncontrollable shock to the tail disrupts both the capacity for instrumental learning and the recovery of locomotor function following spinal cord injury (SCI). Whereas evidence suggests that the disruption of instrumental learning depends on maladaptive plasticity within spinal cord neurons, it is still unknown whether the disruptive effects of shock on locomotor recovery following SCI reflects a brain or spinally-mediated effect. The present experiments address this research question by determining whether shock exposure induces an alteration within the spinal cord of contused rats and testing the effects of disrupting communication between the spinal cord and brain during shock exposure to see if this manipulation protects animals from the effects of shock on locomotor recovery. Experiment 1 found that contused rats transected prior to shock exposure failed to acquire the instrumental response when tested 24 hours later. In addition, contused animals transected after shock exposure also failed to learn when tested, though this effect was less robust. Given the results of Experiment 1, it is plausible that impaired spinal function is sufficient to explain the effects of shock on locomotor recovery. Experiments 2 and 3 addressed this possibility by manipulating communication between the brain and spinal cord prior to shock exposure. In Experiment 2 intrathecal lidocaine was applied rostral to the injury to temporarily disrupt transmission. In Experiment 3, normal brain function was inhibited with intraperitoneal injection of pentobarbital. Interestingly, both manipulations showed that disrupting normal communication between the spinal cord and brain during shock exposure protected animals from the adverse consequences of shock on locomotor recovery. The data suggest that, following SCI, blocking communication between the brain and spinal cord protects animals from the adverse consequences of uncontrollable stimulation.

Prior studies have shown that exposure to uncontrollable stimulation can have a variety of adverse consequences on plasticity. For example, as little as 30 min of uncontrollable shock to the tail disrupts both the capacity for instrumental learning and the recovery of locomotor function following spinal cord injury (SCI). Whereas evidence suggests that the disruption of instrumental learning depends on maladaptive plasticity within spinal cord neurons, it is still unknown whether the disruptive effects of shock on locomotor recovery following SCI reflects a brain or spinally-mediated effect. The present experiments address this research question by determining whether shock exposure induces an alteration within the spinal cord of contused rats and testing the effects of disrupting communication between the spinal cord and brain during shock exposure to see if this manipulation protects animals from the effects of shock on locomotor recovery. Experiment 1 found that contused rats transected prior to shock exposure failed to acquire the instrumental response when tested 24 hours later. In addition, contused animals transected after shock exposure also failed to learn when tested, though this effect was less robust. Given the results of Experiment 1, it is plausible that impaired spinal function is sufficient to explain the effects of shock on locomotor recovery. Experiments 2 and 3 addressed this possibility by manipulating communication between the brain and spinal cord prior to shock exposure. In Experiment 2 intrathecal lidocaine was applied rostral to the injury to temporarily disrupt transmission. In Experiment 3, normal brain function was inhibited with intraperitoneal injection of pentobarbital. Interestingly, both manipulations showed that disrupting normal communication between the spinal cord and brain during shock exposure protected animals from the adverse consequences of shock on locomotor recovery. The data suggest that, following SCI, blocking communication between the brain and spinal cord protects animals from the adverse consequences of uncontrollable stimulation.

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Thesis (M.A.Sc.)--University of Toronto, 2005.