• Jun Wang, Xu Zhang, Bing Cao, Jin Liu, and Ying Li.
• Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
• Cereb. Cortex. 2015 Apr 1;25(4):859-68.

AbstractElectrophysiological studies have shown the enhanced response of anterior cingulate cortex (ACC) to colorectal distension in viscerally hypersensitive (VH) rats, which can be observed up to 7 weeks following colonic anaphylaxis, independent of colon inflammation, suggesting a mechanism for learning and triggering of pain memories in the ACC neuronal circuitry. Activity-dependent plasticity in synaptic strength may serve as a key mechanism that reflects cortical plasticity. However, only a few reports have indicated the synaptic plasticity of ACC in vivo. In the present study, electrophysiological recording showed long-lasting potentiation of local field potential in the medial thalamus (MT)-ACC synapses in VH rats. Theta burst stimulation in the MT reliably induced long-term potentiation in the MT-ACC pathway in normal rats, but was occluded in the VH state. Further, repeated tetanization of MT increased ACC neuronal activity and visceral pain responses of normal rats, mimicking VH rats. In conclusion, we demonstrated for the first time that visceral hypersensitivity is associated with alterations of synaptic plasticity in the ACC. The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.© The Author 2013. Published by Oxford University Press.

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