%0 Journal Article %A Prisca Honoré %A Patrick M. Menning %A Scott D. Rogers %A Michael L. Nichols %A Allan I. Basbaum %A Jean-Marie Besson %A Patrick W. Mantyh %T Spinal Substance P Receptor Expression and Internalization in Acute, Short-Term, and Long-Term Inflammatory Pain States %D 1999 %R 10.1523/JNEUROSCI.19-17-07670.1999 %J The Journal of Neuroscience %P 7670-7678 %V 19 %N 17 %X 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. %U https://www.jneurosci.org/content/jneuro/19/17/7670.full.pdf