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The spinal cord is the gateway for information transfer between body and brain but is not simply a conduit. Within its central gray matter lie millions of neurons that integrate and coordinate complex sensory, motor and autonomic events. Spinal cord injuries can permanently sever descending command pathways and produce paralysis. After some time the injured cord often become hyper-responsive and may result in spasticity (hyperreflexia), autonomic dysfunction and devastating chronic pain syndromes. Brain modulatory systems regulate spinal cord excitability and it may be disruption of their actions that are primarily responsible for the hyperactivity seen after cord injury or in diseases states. A major goal of our lab is to understand how the major brain monoamine modulatory transmitters (serotonin, dopamine, and nor-adrenaline) regulate cord function. These transmitters have been linked to activation of the spinal cord circuitry generating locomotion, control of autonomic NS function, as well as the potent inhibition of spinal cord pain systems. Dysfunction is spinal dopamine is also strongly implicated in the emergence of Restless Legs Syndrome (RLS). We are also very interested in additional mechanisms that limit body sensations. Current research in the lab focuses on: 1. Non-classical control of body sensations. 2. Restless Legs Syndrome (RLS) and spinal cord dopamine. 3. Plasticity of spinal cord function after injury. 4. Regulation of spinal cord locomotor activity. 5. Unusual modulatory mechanisms controlling spinal cord function.