Interleukin-1beta increases spinal cord wind-up activity in normal but not in monoarthritic rats.

Cytokines produced by spinal cord glia after peripheral inflammation, infection or trauma have a relevant role in the maintenance of pain states. The effect of intrathecally administered interleukin-1beta (IL-1beta) on spinal cord nociceptive transmission was studied in normal and monoarthritic rats by assessing wind-up activity in a C-fiber-mediated reflex paradigm evoked by repetitive (1 Hz) electric stimulation. Low i.t. doses of IL-1beta (0.03, 0.12, 0.5 and 2.0 ng) dose-dependently enhanced wind-up activity in normal rats, while higher doses (8.0 ng) only produced a marginal unsignificant effect. IL-1beta administration to monoarthritic rats did not significantly change wind-up scores at any dose. Adaptive changes developed in the spinal cord during chronic pain may underlie the ineffectiveness of exogenous IL-1beta to up-regulate nociceptive transmission.