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Neural Plasticity
Volume 2016, Article ID 3898924, 8 pages
Research Article

Rostral Agranular Insular Cortex Lesion with Motor Cortex Stimulation Enhances Pain Modulation Effect on Neuropathic Pain Model

1Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea
2Brain Korea 21 PLUS Project for Medical Science and Brain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea
3Department of Electrical and Computer Engineering, College of Engineering, Seoul National University, Seoul, Republic of Korea
4Department of Physiology, Hallym University College of Medicine, Chuncheon, Republic of Korea

Received 17 June 2016; Revised 29 August 2016; Accepted 26 September 2016

Academic Editor: Long-Jun Wu

Copyright © 2016 Hyun Ho Jung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is well known that the insular cortex is involved in the processing of painful input. The aim of this study was to evaluate the pain modulation role of the insular cortex during motor cortex stimulation (MCS). After inducing neuropathic pain (NP) rat models by the spared nerve injury method, we made a lesion on the rostral agranular insular cortex (RAIC) unilaterally and compared behaviorally determined pain threshold and latency in 2 groups: Group A (NP + MCS; ) and Group B (NP + RAIC lesion + MCS; ). Also, we simultaneously recorded neuronal activity (NP; ) in the thalamus of the ventral posterolateral nucleus and RAIC to evaluate electrophysiological changes from MCS. The pain threshold and tolerance latency increased in Group A with “MCS on” and in Group B with or without “MCS on.” Moreover, its increase in Group B with “MCS on” was more than that of Group B without MCS or of Group A, suggesting that MCS and RAIC lesioning are involved in pain modulation. Compared with the “MCS off” condition, the “MCS on” induced significant threshold changes in an electrophysiological study. Our data suggest that the RAIC has its own pain modulation effect, which is influenced by MCS.