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Effects of Electroacupucture on NMDA Receptor-dependent Spinal ERK MAPK Expression in CFA-induced Pain Model  

Kim, Ha-Neui (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University)
Kim, Yu-Ri (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University)
Jang, Ji-Yeon (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University)
Choi, Yung-Hyun (Department of Biochemistry, College of Oriental Medicine, Dongeui University)
Lee, Yong-Tae (Department of Physiology, College of Oriental Medicine, Dongeui University)
Choi, Byung-Tae (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.24, no.6, 2010 , pp. 983-988 More about this Journal
Abstract
The present study aims to investigate a possible mechanism of electroacupuncture (EA) in the spinal dorsal horn that may underlie N-methyl-D-aspartate (NMDA) receptor-associated extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) signaling pathways. The hot plate latency of the ipsilateral hindpaw of EA-treated rats was significantly decreased compared with complete Freund's adjuvant (CFA)-injected ones. The expressions of NR1 and NR2B subuint mRNA of NMDA receptor in the whole L4-5 segments are decreased by CFA treatment, but NR2B subunit was significantly recovered by EA treatment. When we detected the expression of ERK, there were no significant difference between normal and CFA-treated rats with EA or NMDA receptor antagonist MK801. But phosphorylated ERK expressions were markedly induced by CFA, but these inductions were significantly modulated by EA treatment. Although hosphorylation of ERK was also arrested by MK801, these inductions of CFA-injected rats was markedly inhibited only by co-treatment with EA and MK801. Phosphorylated cAMP response element-binding protein (CREB), ERK-related transcriptional factor, showed a significant increase in CFA-treated rats and this increase was slightly inhibited by EA and MK801 treatments. But immunoreaction for phosphorylated CREB were significantly increased by CFA treatment in the superficial laminae of the dorsal horn and these inductions were significantly arrested by co-treatment of EA and MK801. Consequently, the hyperalgesia induced by CFA are associated NMDA receptor and EA and MK801 may showed anti-hyperalgesia via same mechanism for inhibition of ERK and CREB phosphorylation in the dorsal horn.
Keywords
NMDA receptor; ERK; MK801; CREB;
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