Rostral Agranular Insular Cortex Lesion with Motor Cortex Stimulation Enhances Pain Modulation Effect on Neuropathic Pain Model.
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;n= 7) and Group B (NP + RAIC lesion + MCS;n= 7). Also, we simultaneously recorded neuronal activity (NP;n= 9) 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.
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyun Ho
HH
Jung
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea; Brain Korea 21 PLUS Project for Medical Science and Brain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jaewoo
0000-0002-6335-1292
J
Shin
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jinhyung
0000-0002-7501-3522
J
Kim
Department of Electrical and Computer Engineering, College of Engineering, Seoul National University, Seoul, Republic of Korea.
Seung-Hee
SH
Ahn
Department of Electrical and Computer Engineering, College of Engineering, Seoul National University, Seoul, Republic of Korea.
Sung Eun
SE
Lee
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea; Department of Physiology, Hallym University College of Medicine, Chuncheon, Republic of Korea.
Chin Su
0000-0003-2115-7894
CS
Koh
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jae Sung
0000-0002-6290-2195
JS
Cho
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Chanho
C
Kong
Department of Physiology, Hallym University College of Medicine, Chuncheon, Republic of Korea.
Hyung-Cheul
HC
Shin
Department of Electrical and Computer Engineering, College of Engineering, Seoul National University, Seoul, Republic of Korea.
Sung June
SJ
Kim
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea; Brain Korea 21 PLUS Project for Medical Science and Brain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jin Woo
0000-0002-2717-0101
JW
Chang
D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D008297:Male; D009044:Motor Cortex / Q000503:physiopathology*; D009437:Neuralgia / Q000503:physiopathology*; D010147:Pain Measurement; D017288:Pain Threshold / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000503:physiopathology
D016760:Proto-Oncogene Proteins c-fos