Nociceptive nerve impulses generated in peripheral tissues are conducted by sensory fibers to the superficial spinal dorsal horn. Following local processing, the nociceptive signals are transmitted to higher brain centers through ascending sensory pathways. In higher brain centers, the nociceptive signals evoke various motivational-affective behaviors including pain. Due to chronic inflammatory processes the nociceptive sensory system undergoes a chemical reorganization resulting in central sensitization and chronic pain.

The major goal of our experiments was to study the spinal expression of IL-1b and the ligand binding subunit of its receptor (interleukin-1 receptor type 1 /IL-1R1/) in the Freund adjuvant–induced inflammatory pain model. In this model chronic pain was induced by subcutaneous injection of complete Freund adjuvant (CFA) into the hindpaw of Wistar rats (n=9). Mechanical allodynia indicating the development of chronic pain was measured by the modified von Frey test. On each experimental day (0–3 days) animals were sacrificed (n=3/ day) and protein was extracted from the dorsal horn of spinal cord to measure relative protein levels by western blot technique. At the peak of mechanical allodynia (day 3) we studied the expressional pattern of the IL1 receptor and its ligand IL1b by immunohistochemical method. Western blot results show gradual elevation of IL-1R1 during the course of the model. While confocal microscopy shows that IL-1R1 was expressed not only on neurons, but also by astrocytes and microglial cells. IL1b was found to be remarkably up-regulated in the spinal astrocytes and to a lesser amount it is produced by microglia.

Our results suggest that the IL-1R1 and the IL-1b contribute to neuronal-glial interactions, and the development of chronic inflammatory pain.