Jun-Ho La

Jun-Ho La, PhD, DVM is an Associate Professor in the Department of Neurobiology at the University of Texas Medical Branch (UTMB). His research program focuses on elucidating mechanisms of chronic pain chronification, particularly nociplastic pain transitions without persistent tissue injury, using multidisciplinary approaches including behavioral, molecular, electrophysiological, and imaging techniques.

His educational background includes a DVM, MS, and PhD in Veterinary Physiology from Seoul National University, followed by postdoctoral training at Gyeongsang National University and the University of Pittsburgh. His work bridges veterinary medicine and human pain research through comparative neurobiological studies.

Dr. La's research interests center on nociplastic pain mechanisms, visceral pain pathways, and synaptic plasticity in nociceptive circuits. His lab investigates how oxidative stress, ion channels (particularly K2P channels), and glial cells contribute to pain chronification. A key focus is understanding sex-specific pain mechanisms and developing non-opioid therapeutic strategies targeting peripheral and central sensitization.

Analysis of his 15 most recent publications reveals a consistent trajectory toward understanding nociplastic pain transitions, with increasing emphasis on sex differences, neuromodulation techniques like spinal cord stimulation, and novel therapeutic targets including GPR37 and AVPR1A receptors. His work demonstrates strong translational potential for managing treatment-resistant chronic pain conditions.

Dr. La has made significant contributions to understanding sensory pathway specialization in visceral organs, particularly the differential roles of vagal, splanchnic, and pelvic nerve pathways in pain signaling. His laboratory has developed critical animal models for studying functional bowel disorders and chemotherapy-induced neuropathy.

His research program integrates cutting-edge techniques including optogenetics, chemogenetics, and Ca²⁺-imaging to dissect pain mechanisms at cellular and circuit levels. Current work emphasizes the development of neuromodulation strategies to prevent acute-to-chronic pain transitions, with particular focus on spinal GABAergic disinhibition and microglial activation pathways.