PT - JOURNAL ARTICLE AU - Prisca Honoré AU - Patrick M. Menning AU - Scott D. Rogers AU - Michael L. Nichols AU - Allan I. Basbaum AU - Jean-Marie Besson AU - Patrick W. Mantyh TI - Spinal Substance P Receptor Expression and Internalization in Acute, Short-Term, and Long-Term Inflammatory Pain States AID - 10.1523/JNEUROSCI.19-17-07670.1999 DP - 1999 Sep 01 TA - The Journal of Neuroscience PG - 7670--7678 VI - 19 IP - 17 4099 - http://www.jneurosci.org/content/19/17/7670.short 4100 - http://www.jneurosci.org/content/19/17/7670.full SO - J. Neurosci.1999 Sep 01; 19 AB - 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.