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 resu lted in a significant enhancement of electrically evoked substance P-l ike immunoreactivity with a maximal effect (> 2-fold increase) at 0.1 ng/ml, whereas higher concentration (10-50 ng/ml) of the cytokine inhi bited (approximate to 50%) the release of the neuropeptide. Interleuki n-1 beta (0.1 ng/ml) potentiation of substance P-like immunoreactivity release was abrogated by co-perfusion with interleukin-l receptor ant agonist (10-100 ng/ml) or with indomethacin (1 mu M) Superfusion of sp inal cord with interleukin-1 beta inhibited electrically evoked calcit onin gene-related peptide-like immunoreactivity release. Modulation of substance P-like immunoreactivity release from the spinal cord by int erleukin-1 beta may represent a mechanism responsible for the hyperalg esic action of the cytokine characteristic of the inflammatory respons e.