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

Interleukin-1β (IL-1β) plays an important role in neuroprotective and neurodegenerative events in the central nervous system. To clarify the mechanism of controversial actions of IL-1β, we determined the effect of IL-1β, as well as the interaction between IL-1β 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-1β increased both adenosine releases, whereas higher concentration did not affect their releases. The stimulatory effect of IL-1β on basal adenosine release was reduced by removal of extracellular Ca2+ and IP3 receptor inhibitor, while the stimulatory effect of IL-1β on K+-stimulated adenosine release was reduced by ryanodine receptor inhibitor. These results suggest that the potent effect of IL-1β upon adenosine release might contribute to the neuroprotective action of IL-1β, whereas IL-1β-induced neurodegeneration might be due to the overload response of Ca2+ mobilization and the inactivation of adenosine exocytosis.