Journal of Physiology & Pathology in Korean Medicine (동의생리병리학회지)

The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine (대한동의생리학회·한의병리학회)
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Effect of Electroacupuncture on AMPA Receptor GluR2 Subunit in Complete Freund's Adjuvant-induced Inflammatory Pain Model

  • Kim, Chul-Yun (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University) ;
  • Choi, Hye-Young (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University) ;
  • Yang, Yeun-Jin (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University) ;
  • Choi, Byung-Tae (Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University)
  • Received : 2011.08.04
  • Accepted : 2011.09.15
  • Published : 2011.10.25
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Abstract

AMPA receptor (AMPAR)s are heterotetrameric structures made up from 4 units (GluR1-4) and are thought to underlie perception of persistent inflammatory pain. Complete Freund's adjuvant (CFA)-evoked inflammation induces synaptic GluR2 internalization, which is initiated by GluR2 phosphorylation, in dorsal horn neurons during the maintenance of CFA-induced hypersensitivity. The present study investigated whether electroacupuncture (EA) stimulation has any effect on GluR2 trafficking by using immunoblot and immunohistochemistry. We examined that CFA-induced dorsal horn GluR2 internalization was attenuated by EA treatment. EA treatment could also decrease the level of pGluR2 regardless of whether CFA injection was administrated or not. In addition, previous studies suggest that microglial cells are increased without morphological change in CFA injected animal. In our study, increases in microglial cells in CFA group were observed, whereas EA with or without CFA-injected group showed similar aspects with normal group. In conclusion, our results indicate that EA might blunt CFA-evoked inflammation by coordinating mechanisms at the upstream step of neuron activation and GluR2 phosphorylation.

Keywords

References

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