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이배환(생리학교실) Sci Rep
등록일 : 2017-08-14 오전 10:26:00       조회 : 159
첨   부 :
제1저자 차명훈(생리학교실)
교신저자 이배환(생리학교실, BK21)

Sci Rep. 2017 Aug 11ɕ(1):7986. doi: 10.1038/s41598-017-08208-2.
Repetitive motor cortex stimulation reinforces the pain modulation circuits of peripheral neuropathic pain.
Cha M1, Um SW1,2, Kwon M1,2, Nam TS1, Lee BH3,4.

Author information

1Department of Physiology, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.2Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.3Department of Physiology, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea. bhlee@yuhs.ac.4Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea. bhlee@yuhs.ac.

Abstract

Recent evidence indicates that motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. However, the neural mechanisms underlying the attenuated hyperalgesia after MCS are not completely understood. In this study, we investigated the neural mechanism of the effects of MCS using an animal model of neuropathic pain. After 10 daily sessions of MCS, repetitive MCS reduced mechanical allodynia and contributed to neuronal changes in the anterior cingulate cortex (ACC). Interestingly, inhibition of protein kinase M zeta (PKMζ), a regulator of synaptic plasticity, in the ACC blocked the effects of repetitive MCS. Histological and molecular studies showed a significantly increased level of glial fibrillary acidic protein (GFAP) expression in the ACC after peripheral neuropathy, and neither MCS treatment nor ZIP administration affected this increase. These results suggest that repetitive MCS can attenuate the mechanical allodynia in neuropathic pain, and that the activation of PKMζ in the ACC may play a role in the modulation of neuropathic pain via MCS.
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