I have a long-standing research interest in chronic pain and developing therapeutic tools to manage this debilitating condition. My current research focuses on mechanisms of pain chronification, namely transition from acute to chronic pain, without underlying persistent tissue injury. This type of chronic pain is recently termed 'nociplastic pain', implying persistent plastic changes in the nociceptive neural circuit itself in this chronic pain state. There is growing appreciation that changes in synaptic strength (i.e., synaptic plasticity) are associated with chronic pain, and primary afferent input dynamically contributes to synaptic plasticity in spinal nociceptive circuit. Using behavioral, molecular biological, electrophysiological, and Ca2+-imaging approaches combined with optogenetic and chemogenetic tools, my lab investigates such long-term changes in peripheral and central nociceptive circuit components including non-neuronal cells (e.g., spinal glia).
I have also studied chronic visceral pain associated with inflammatory diseases as well as functional bowel disorders. Visceral organs are innervated by at least two different sensory pathways (e.g., vagal and splanchnic nerve pathways for upper visceral organs, and lumbar splanchnic and pelvic nerve pathways for lower pelvic organs), and my work has contributed to understanding of the characteristics of these different sensory pathways by, for example, examining their ion channel expression and electrophysiological properties. In addition, my research goal to identify potential therapeutic targets led me to development and characterization of animal models of visceral pain, and discoveries of important roles of two-pore domain K+ (K2P) channels in primary afferent neurons and condition-specific involvement of colonic inflammatory molecules in visceral hypersensitivity.
Publications/Creative Works
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Affiliations
Research Consortia
Gulf Coast Consortium for Translational Pain Research
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