Effect of interleukin-1 beta on the release of substance P from rat isolated spinal cord.
Superfusion of rat spinal cord slices with rat interleukin-1 beta resulted in a significant enhancement of electrically evoked substance P-like immunoreactivity with a maximal effect (> 2-fold increase) at 0.1 ng/ml, whereas higher concentration (10-50 ng/ml) of the cytokine inhibited (approximately 50%) the release of the neuropeptide. Interleukin-1 beta (0.1 ng/ml) potentiation of substance P-like immunoreactivity release was abrogated by co-perfusion with interleukin-1 receptor antagonist (10-100 ng/ml) or with indomethacin (1 microM). Superfusion of spinal cord with interleukin-1 beta inhibited electrically evoked calcitonin gene-related peptide-like immunoreactivity release. Modulation of substance P-like immunoreactivity release from the spinal cord by interleukin-1 beta may represent a mechanism responsible for the hyperalgesic action of the cytokine characteristic of the inflammatory response.
Malcangio
M
M
Department of Pharmacology, School of Pharmacy, London, UK.
Bowery
N G
NG
Flower
R J
RJ
Perretti
M
M
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology; D012795:Sialoglycoproteins / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects* / Q000378:metabolism; D013373:Substance P / Q000378:metabolism*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D011994:Recombinant Proteins; D012795:Sialoglycoproteins; D013373:Substance P; D015740:Calcitonin Gene-Related Peptide; D007213:Indomethacin