Prior work has demonstrated that spinal cord neurons, isolated from the brain through a spinal transection, can support learning. Spinally transected rats given legshock whenever one hindlimb is extended learn to maintain the shocked leg in a flexed position, minimizing net shock exposure. This capacity for learning is inhibited by prior exposure to an uncontrollable stimulus (e.g., intermittent tailshock). The present experiments examined whether spinal cord neurons are more vulnerable to the adverse effects of uncontrollable stimulation after spinal cord injury. Experiment 1 confirmed that uncontrollable shock inhibits subsequent learning in transected rats. Rats that received uncontrollable stimulation prior to transection did not exhibit this effect, suggesting that brain systems exert a protective effect. Experiment 2 showed that this protective effect was removed if subjects received a dorsolateral funiculus lesion prior to shock exposure. Subsequent experiments were designed to determine the identity of the neurochemical systems that protect spinal plasticity. Intrathecal application of serotonin (5-HT) or a 5-HT 1A/7 agonist (8-OH DPAT) in transected rats had a protective effect that blocked the adverse effect of uncontrollable stimulation (Experiment 3). The alpha-2 noradrenergic agonist, clonidine, also protected plasticity (Experiment 4), but this effect was linked to cross-reactivity at the 5-HT 1A receptor (Experiment 5). Microinjection of a 5HT 1A antagonist (WAY 100635) into the spinal cord before intact rats received uncontrollable stimulation blocked the brain-dependent protection of spinal cord neurons. The findings indicate that serotonergic systems normally protect spinal cord plasticity from the deleterious effects of uncontrollable stimulation.
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