Abstract

Event Abstract Back to Event Genetic and synaptic studies of pain-related central plasticity in the anterior cingulate cortex Min Zhuo1* 1 University of Toronto, Department of Physiology, Canada Investigation of molecular and cellular mechanisms of synaptic plasticity is the major focus of many neuroscientists. There are two major reasons for searching new genes and molecules contributing to central plasticity: first, it provides basic neural mechanism for learning and memory, a key function of the brain; second, it provides new targets for treating brain-related disease. LTP, mostly intensely studied in the hippocampus and amygdala, is proposed to be a cellular model for learning and memory. In our recent studies, we have established LTP in the anterior cingulate cortex (ACC) as a cellular model for chronic pain in the brain. We have demonstrated that peripheral injury (e.g., amputation, inflammation or nerve injury) caused long-lasting enhancement of excitatory synaptic transmission in the ACC pyramidal cells. Such potentiation or LTP is independent of peripheral sensory inputs once it has been established. By using integrative approaches including genetic, pharmacological and physiological studies, we have systemically characterized excitatory synaptic transmission and synaptic plasticity (including LTP and LTD) in the ACC cells. We found that NMDA receptor-dependent signaling pathways are important for ACC LTP. Our recent ongoing studies further showed that injury triggered both presynaptic increases of glutamate release and postsynaptic enhancement of glutamate AMPA receptor mediated responses. We have identified NMDA NR2B receptor as well as calcium-stimulated adenylyl-cyclase subtype AC1 as key-signaling proteins for injury-related plasticity in the ACC neurons.Our recent preliminary observations suggest that peripheral injury also triggered changes in intrinsic plasticity of ACC pyramidal cells. Based on these findings, I thus propose that ACC LTP may serve as a cellular model for studying cortical sensitization that related to chronic pain, as well as pain-related cognitive emotional disorders (Zhuo, 2008, Trends in Neuroscience). Understanding signaling pathways related to ACC LTP may help us to identify novel drug targets for treating chronic pain and related mental disorders. Conference: 11th Meeting of the Portuguese Society for Neuroscience, Braga, Portugal, 4 Jun - 6 Jun, 2009. Presentation Type: Oral Presentation Topic: Plenary lectures Citation: Zhuo M (2009). Genetic and synaptic studies of pain-related central plasticity in the anterior cingulate cortex. Front. Neurosci. Conference Abstract: 11th Meeting of the Portuguese Society for Neuroscience. doi: 10.3389/conf.neuro.01.2009.11.004 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2009; Published Online: 04 Aug 2009. * Correspondence: Min Zhuo, University of Toronto, Department of Physiology, Toronto, Canada, min.zhuo@utoronto.ca Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Min Zhuo Google Min Zhuo Google Scholar Min Zhuo PubMed Min Zhuo Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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