Upregulation of forebrain NMDA NR2B receptors contributes to behavioral sensitization after inflammation

J Neurosci. 2005 Nov 30;25(48):11107-16. doi: 10.1523/JNEUROSCI.1678-05.2005.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal
  • Excitatory Postsynaptic Potentials
  • Freund's Adjuvant
  • Gyrus Cinguli / metabolism*
  • Gyrus Cinguli / physiopathology
  • Hyperalgesia / etiology*
  • Hyperalgesia / psychology
  • Inflammation / chemically induced
  • Inflammation / complications*
  • Inflammation / metabolism*
  • Inflammation / physiopathology
  • Mice
  • Mice, Inbred C57BL
  • Nociceptors / physiopathology
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Synapses
  • Synaptic Transmission
  • Up-Regulation*


  • NR2B NMDA receptor
  • Receptors, N-Methyl-D-Aspartate
  • Freund's Adjuvant