To determine whether interleukin-1β (IL-1β) in the brain may modulate nociception, recombinant human IL-1β (rhIL-1β) (1pg/kg to 1 μg/kg) was microinjected into lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 ± 0.1°C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1β, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1β to > 1 ng/kg (up to 1 μg/kg had no effect on the nociceptive threshold. The rhIL-1β-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with α-melanocyte-stimulating hormone (α-MSH) also inhibited the rhIL-1β-induced hyperalgesia. However, pretreatment with α-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1β in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to α-MSH. The hyperalgesic action of central IL-1 does not appear to depende on the CRF system.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology