Korean J Physiol Pharmacol 2022; 26(2): 69-75
Published online March 1, 2022 https://doi.org/10.4196/kjpp.2022.26.2.69
Copyright © Korean J Physiol Pharmacol.
Yoo Rim Kim1,3 and Sang Jeong Kim1,2,3,*
Departments of 1Physiology, 2Biomedical Sciences, Seoul National University College of Medicine, 3Neuroscience Research Institute, Seoul National University College of Medicine, Seoul 03080, Korea
Correspondence to:Sang Jeong Kim
E-mail: sangjkim@snu.ac.kr
This is an Open Access journal distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Chronic pain is induced by tissue or nerve damage and is accompanied by pain hypersensitivity (i.e., allodynia and hyperalgesia). Previous studies using in vivo two-photon microscopy have shown functional and structural changes in the primary somatosensory (S1) cortex at the cellular and synaptic levels in inflammatory and neuropathic chronic pain. Furthermore, alterations in local cortical circuits were revealed during the development of chronic pain. In this review, we summarize recent findings regarding functional and structural plastic changes of the S1 cortex and alteration of the S1 inhibitory network in chronic pain. Finally, we discuss potential neuromodulators driving modified cortical circuits and suggest further studies to understand the cortical mechanisms that induce pain hypersensitivity.
Keywords: Chronic pain, Cortical circuit, Inhibitory network, Neuropathic pain, Primary somatosensory cortex
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