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The Journal of Neuroscience, November 30, 2005, 25(48):11107-11116; doi:10.1523/JNEUROSCI.1678-05.2005

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Cellular/Molecular
Upregulation of Forebrain NMDA NR2B Receptors Contributes to Behavioral Sensitization after Inflammation

Long-Jun Wu,¹ Hiroki Toyoda,¹ Ming-Gao Zhao,¹ Yong-Seok Lee,⁶ Jianrong Tang,¹ Shanelle W. Ko,¹ Yong Heng Jia,¹ Fanny W. F. Shum,¹ Celina V. Zerbinatti,² Guojun Bu,² Feng Wei,¹ Tian-Le Xu,⁴ Louis J. Muglia,² Zhou-Feng Chen,³ Yves P. Auberson,⁵ Bong-Kiun Kaang,⁶ and Min Zhuo¹

¹Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, Toronto, Ontario, Canada M5S 1A8, Departments of ²Pediatrics, Anesthesiology, Psychiatry, and Molecular Biology and ³Pharmacology, Washington University in St. Louis, St. Louis, Missouri 63110, ⁴Institute of Neuroscience, Chinese Academy of Sciences, Shanghai 200031, China, ⁵Novartis Institutes of Biomedical Research, Novartis Pharma AG, CH-4002 Basel, Switzerland, and ⁶Department of Biological Sciences, Seoul National University, Seoul 151-742, Korea

Transgenic 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.

Key words: NMDA receptors; NR2B; anterior cingulate cortex; inflammation; pain; hyperalgesia

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Received April 27, 2005; revised October 18, 2005; accepted October 18, 2005.

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