Involvement of Ca(2+)-induced Ca2+ releasing system in interleukin-1beta-associated adenosine release |
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Authors: | Zhu Gang Okada Motohiro Yoshida Shukuko Mori Fumiaki Hirose Shinichi Wakabayashi Koichi Kaneko Sunao |
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Affiliation: | Department of Neuropsychiatry, Hirosaki University School of Medicine, Hirosaki 036-8562, Japan. |
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Abstract: | Interleukin-1beta (IL-1beta) plays an important role in neuroprotective and neurodegenerative events in the central nervous system. To clarify the mechanism of controversial actions of IL-1beta, we determined the effect of IL-1beta, as well as the interaction between IL-1beta and Ca(2+)-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-1beta increased both adenosine releases, whereas higher concentration did not affect their releases. The stimulatory effect of IL-1beta on basal adenosine release was reduced by removal of extracellular Ca2+ and IP3 receptor inhibitor, while the stimulatory effect of IL-1beta on K(+)-stimulated adenosine release was reduced by ryanodine receptor inhibitor. These results suggest that the potent effect of IL-1beta upon adenosine release might contribute to the neuroprotective action of IL-1beta, whereas IL-1beta-induced neurodegeneration might be due to the overload response of Ca2+ mobilization and the inactivation of adenosine exocytosis. |
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Keywords: | Interleukin-1β Adenosine Ca2+-induced Ca2+ releasing system Neuroprotection Neurodegeneration Hippocampus |
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