• Kohei Koga, Giannina Descalzi, Tao Chen, Hyoung-Gon Ko, Jinshan Lu, Shermaine Li, Junehee Son, TaeHyun Kim, Chuljung Kwak, Richard L Huganir, Ming-Gao Zhao, Bong-Kiun Kaang, Graham L Collingridge, and Min Zhuo.
• Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada.
• Neuron. 2015 Jan 21;85(2):377-89.

AbstractChronic pain can lead to anxiety and anxiety can enhance the sensation of pain. Unfortunately, little is known about the synaptic mechanisms that mediate these re-enforcing interactions. Here we characterized two forms of long-term potentiation (LTP) in the anterior cingulate cortex (ACC); a presynaptic form (pre-LTP) that requires kainate receptors and a postsynaptic form (post-LTP) that requires N-methyl-D-aspartate receptors. Pre-LTP also involves adenylyl cyclase and protein kinase A and is expressed via a mechanism involving hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. Interestingly, chronic pain and anxiety both result in selective occlusion of pre-LTP. Significantly, microinjection of the HCN blocker ZD7288 into the ACC in vivo produces both anxiolytic and analgesic effects. Our results provide a mechanism by which two forms of LTP in the ACC may converge to mediate the interaction between anxiety and chronic pain.Copyright © 2015 Elsevier Inc. All rights reserved.

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