Involvement of Ca2+-induced Ca2+ releasing system in interleukin-1β-associated adenosine release

Interleukin-1 beta (IL-1 beta) plays an important role in neuroprotective and neurodegenerative events in the central nervous system. To clarify the mechanism of controversial actions of IL-1 beta, we determined the effect of IL-1 beta, as well as the interaction between IL-1 beta and Ca2+-induced Ca2+ releasing system (CICR), on adenosine releases in mice hippocampus using mini-slices method. Basal and K-stimulated adenosine releases were regulated by two types of CICRs, including inositol-1,4,5-trisphosphate (IP3) receptor and ryanodine receptor. Lower concentration of IL-1 beta increased both adenosine releases, whereas higher concentration did not affect their releases. The stimulatory effect of IL-1 beta on basal adenosine release was reduced by removal of extracellular Ca2+ and IP3 receptor inhibitor, while the stimulatory effect of IL-1 beta on K-stimulated adenosine release was reduced by ryanodine receptor inhibitor. These results suggest that the potent effect of IL-1 beta upon adenosine release might contribute to the neuroprotective action of IL-1 beta, whereas IL-1 beta-induced neurodegeneration might be due to the overload response of Ca2+ mobilization and the inactivation of adenosine exocytosis. (c) 2006 Elsevier B.V. All rights reserved.