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Sci. STKE, 11 May 2004
Vol. 2004, Issue 232, p. tw172
[DOI: 10.1126/stke.2322004TW172]

EDITORS' CHOICE

NEUROBIOLOGY Processing Inflammatory Pain

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 {alpha}3 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 {alpha}3: 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]

Citation: Processing Inflammatory Pain. Sci. STKE 2004, tw172 (2004).

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