Genetic enhancement of inflammatory pain by forebrain NR2B overexpression

F. Wei, G. D. Wang, G. A. Kerchner, S. J. Kim, H. M. Xu, Z. F. Chen, M. Zhuo

Research output: Contribution to journalArticlepeer-review

268 Scopus citations


N-methyl-D-aspartate (NMDA) receptors contribute to many brain functions. We studied the effect of forebrain-targeted overexpression of the NMDA receptor subunit NR2B on the response of mice to tissue injury and inflammation. Transgenic mice exhibited prominent NR2B expression and enhanced NMDA receptor-mediated synaptic responses in two pain-related forebrain areas, the anterior cingulate cortex and insular cortex, but not in the spinal cord. Although transgenic and wild type mice were indistinguishable in tests of acute pain, transgenic mice exhibited enhanced responsiveness to peripheral injection of two inflammatory stimuli, formalin and complete Freund's adjuvant. Genetic modification of forebrain NMDA receptors can therefore influence pain perception, which suggests that forebrain-selective NMDA receptor antagonists, including NR2B-selective agents, may be useful analgesics for persistent pain.

Original languageEnglish
Pages (from-to)164-169
Number of pages6
JournalNature neuroscience
Issue number2
StatePublished - Feb 19 2001


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