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Previous Article | Next Article
The Journal of Neuroscience, September 1, 1999, 19(17):7670-7678
Spinal Substance P Receptor Expression and Internalization in Acute, Short-Term, and Long-Term Inflammatory Pain States
Prisca Honoré1, 2, Patrick M. Menning1, 2, Scott D. Rogers1, 2, Michael L. Nichols1, 2, Allan I. Basbaum3, Jean-Marie Besson4, and Patrick W. Mantyh1, 2 1 Neurosystems Center, Department of Preventive Sciences, Psychiatry and Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455, 2 Veterans Affairs Medical Center, Minneapolis, Minnesota 55417, 3 Department of Anatomy and Physiology and W. M. Keck Foundation Center for Integrative Neuroscience, University of California, San Francisco, San Francisco, California 94143, and 4 Institut National de la Sante et de la Recherche Medicale U161, 75014 Paris, France
Inflammatory pain involves the sensitization of both primary afferent and spinal cord neurons. To explore the neurochemical changes that contribute to inflammatory pain, we have examined the expression and ligand-induced internalization of the substance P receptor (SPR) in the spinal cord in acute, short-term, and long-term inflammatory pain states. These inflammatory models included unilateral injection of formalin (8-60 min), carrageenan (3 hr), and complete Freund's adjuvant (CFA; 3 d) into the rat hindpaw as well as adjuvant-induced polyarthritis (21 d). In acute inflammatory pain there is ongoing release of substance P (SP) as measured by SPR internalization in lamina I neurons at both 8 and 60 min after formalin injection. Although there is no tonic release of SP in short-term inflammatory pain, at 3 hr after carrageenan injection, SP is released in response to both noxious and non-noxious somatosensory stimulation with SPR internalization being observed in neurons located in both laminae I and III-IV. In long-term inflammatory pain models (CFA and polyarthritis) the same pattern of SP release and SPR activation occurs as is observed in short-term inflammation with the addition that there is a significant upregulation of the SPR in lamina I neurons. These results suggest that SPR internalization might serve as a marker of the contribution of ongoing primary afferent input in acute and persistent pain states. These stereotypical neurochemical changes suggest that there are unique neurochemical signatures for acute, short-term, and long-term inflammatory pain.
Key words: carrageenan; complete Freund adjuvant; formalin; inflammation; internalization; pain; spinal cord; substance P receptor
Copyright © 1999 Society for Neuroscience 0270-6474/99/19177670-09$05.00/0
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