Effect of interleukin-1beta on spinal cord nociceptive transmission of normal and monoarthritic rats after disruption of glial function.

Introduction: Cytokines produced by spinal cord glia after peripheral injuries have a relevant role in the maintenance of pain states. Thus, while IL-1beta is overexpressed in the spinal cords of animals submitted to experimental arthritis and other chronic pain models, intrathecal administration of IL-1beta to healthy animals induces hyperalgesia and allodynia and enhances wind-up activity in dorsal horn neurons.

Methods: To investigate the functional contribution of glial cells in the spinal cord nociceptive transmission, the effect of intrathecally administered IL-1beta was studied in both normal and adjuvant-induced arthritic rats with or without glial inhibition.

Effects of interleukin-1beta on spinal cord nociceptive transmission in intact and propentofylline-treated rats.

To investigate the contribution of glial cells in the spinal cord nociceptive transmission, the effect of intrathecally administered interleukin-1beta (IL-1beta) was studied in rats treated with the glial cell inactivator propentofylline and submitted to a C-fiber-mediated reflex paradigm evoked by single and repetitive (wind-up) electric stimulation. Intrathecal IL-1beta did not modify the C reflex integrated activity in either group of animals, while producing increased wind-up in intact and decreased wind-up in propentofylline pre-treated rats. Results suggest that the excitatory effect of IL-1beta on spinal wind-up activity in healthy rats is produced by a glial mediator, whereas the inhibitory effect resulted from a direct effect of the cytokine on dorsal horn neurons.