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- Long-Jun Wu, Hiroki Toyoda, Ming-Gao Zhao, Yong-Seok Lee, Jianrong Tang, Shanelle W Ko, Yong Heng Jia, Fanny W F Shum, Celina V Zerbinatti, Guojun Bu, Feng Wei, Tian-Le Xu, Louis J Muglia, Zhou-Feng Chen, Yves P Auberson, Bong-Kiun Kaang, and Min Zhuo.
- Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, Toronto, Ontario, M5S 1A8, Canada.
- J. Neurosci. 2005 Nov 30;25(48):11107-16.
AbstractTransgenic overexpression of NMDA NR2B receptors in forebrain regions increased behavioral responses to persistent inflammatory pain. However, it is not known whether inflammation leads to the upregulation of NR2B receptors in these regions. Here, we show that peripheral inflammation increased the expression of NMDA NR2B receptors and NR2B receptor-mediated synaptic currents in the anterior cingulate cortex (ACC). In freely moving mice, the increase in NR2B receptors after inflammation contributed to enhanced NMDA receptor-mediated responses in the ACC. Inhibition of NR2B receptors in the ACC selectively reduced behavioral sensitization related to inflammation. Our results demonstrate that the upregulation of NR2B receptors in the ACC contributes to behavioral sensitization caused by inflammation.
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