Processing Inflammatory Pain

Science's STKE  11 May 2004:
Vol. 2004, Issue 232, pp. tw172-TW172
DOI: 10.1126/stke.2322004TW172

Hyperalgesia, an excessive sensitivity to pain, has been attributed exclusively to a sensitization of peripheral nociceptors. However, changes in the central processing of painful stimuli, particularly in the dorsal horn of the spinal cord, also play an important role. Harvey et al. (see the news story by Marx) show that glycine receptors containing the α3 receptor subtype are primary molecular targets of prostaglandin-induced inflammatory reactions in the spinal cord. Furthermore, inhibition of glycinergic neurotransmission by prostaglandins underlies later stages of inflammatory pain sensitization.

R. J. Harvey, U. B. Depner, H. Wässle, S. Ahmadi, C. Heindl, H. Reinold, T. G. Smart, K. Harvey, B. Schütz, O. M. Abo-Salem, A. Zimmer, P. Poisbeau, H. Welzl, D. P. Wolfer, H. Betz, H. U. Zeilhofer, U. Müller, GlyR α3: An essential target for spinal PGE2-mediated inflammatory pain sensitization. Science 304, 884-887 (2004). [Abstract] [Full Text]

J. Marx, Locating a new step in pain's pathway. Science 304, 811 (2004). [Summary] [Full Text]