My research activities focus on the analysis of neuroplasticity that underlies chronic pain. In one line of research, we are elucidating those receptors involved in the processing of nociceptive (painful) input in the periphery. Then, using models of inflammation coupled with anatomical, behavioral, pharmacological and electrophysiological techniques, we investigate how these receptor populations change in acute and chronic inflammation. We are particularly interested in the role of ionotropic and metabotropic glutamate receptors as well as somatostatin and TRPV1 receptors which are expressed by cutaneous nociceptors. It is becoming clear that a variety of receptors are present on peripheral axons that influence sensory transduction in the normal state and contribute to enhanced nociceptor function in the inflamed state. Investigating neuronal receptor populations in normal skin and changes in these populations in chronic pain states may elucidate new avenues for therapy for pain of peripheral origin. A second focus in the lab is the study of mechanisms underlying both peripheral and central neuropathic pain. Using models of peripheral nerve injury or spinal cord contusion, we are defining those mechanisms contributing to the aberrant sensory processing that arises following PNS or CNS injury, respectively. We have demonstrated that a CNS injury (spinal cord contusion) results in sensitization of primary afferents far from the injury site. This finding may have implications for other painful conditions such as fibromyalgia, thalamic post-stroke pain and migraine pain.
Publications/Creative Works
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Affiliations
Research Consortia
Gulf Coast Consortia for Translational Pain Research
Gulf Coast Cluster for Translational Addiction Science
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