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Abstract

Pain associated with chronic pancreatitis (CP) is frequently severe and refractory to medical and even surgical management. An electroencephalography study suggested that pain in patients with CP was associated with cortical reorganization and anterior cingulate cortex (ACC) neuroplastic changes indicating an important mechanism for learning and triggering of pain memories in the ACC neuronal circuitry in the CP state. In this study we stablish a CP rat model to moniter pancreatic pain and characterize the electrophysiological properties of ACC activated by pancreatic noxious stimuli. We characterized the plasticity in the thalamo-ACC synapse. Chronic pancreatitis suppressed the long-term potentiation (LTP) and disrupted the phase-locking of ACC single neural firings to the ongoing theta oscillation in of local field potential, further interrupted the synchrony in the middle thalamus-ACC pathway. The brain in chronic pain states is not purely receptive but can be viewed as amplifying or possibly even constitutive. In supporting the theory our studies would provide a framework for further clarify how long-term plasticity in the cortex encoding chronic pancreatic pain. Combination of electrophysiology, pharmacology with genetically manipulation in behavioral models in vivo should facilitate to identifying the putative molecular mechanisms underlying the brain cortex sensitization and the memory of chronic pancreatitis pain states.

Biography

Ying Li was a General Surgeon at the Qinghai and Oral-Maxillofacial Surgeon at Nanjing Medical School, China. He has completed his Post-doctoral fellowship in Department of Internal Medicine Hypertension, University of Michigan, where he was appointed as an Assistant Research Scientist in 1997 and Research Professor in the University of Michigan, Medical School Department of Internal Medicine in 2002. He has joined the Department Biomedical Science City, University of Hong Kong in December 2009.

Email: yingli@cityu.edu.hk