Interleukin-10 modulates [Ca²⁺]_i response induced by repeated NMDA receptor activation with brief hypoxia through inhibition of InsP₃-sensitive internal stores in hippocampal neurons

详细信息	查看全文 | 推荐本文 |

• 作者：Marija V. Turovskaya^a ; Egor A. Turovsky^a ; Valery P. Zinchenko^a ; Sergei G. Levin^b ; Oleg V. Godukhin^b ; ^{godukhin@hotmail.com}
• 关键词：Interleukin-10 ; Brief hypoxia ; Cultured hippocampal neurons ; Ca2+ imaging ; Intracellular Ca2+ ; NMDA glutamate receptors ; InsP3-sensitive internal stores ; Ryanodine-sensitive internal stores
• 刊名：Neuroscience Letters
• 出版年：2012
• 期刊代码：52_03043940
• 类别：neu
• 出版时间：10 May, 2012
• 卷：516
• 期：1
• 页码：151-155
• 文件大小：293 K

摘要

The goal of this study was to evaluate an effect of interleukin-10 (IL-10) on the Ca²⁺ response induced by repeated NMDA receptor activation with brief hypoxia in cultured hippocampal neurons. We focused on the importance of internal Ca²⁺ stores in the modulation of this Ca²⁺ response by IL-10. To test this, we compared roles of InsP₃- and ryanodine-sensitive internal stores in the effects of IL-10. Measurements of intracellular cytosolic calcium concentration ([Ca²⁺]_i) in cultured hippocampal neurons were made by imaging Fura-2AM loaded hippocampal cells. Repeated episodes of NMDA receptor activation with brief hypoxia induced the spontaneous (s) [Ca²⁺]_i increases about 3 min after each hypoxic episode. The amplitude of the s[Ca²⁺]_i increases was progressively enhanced from the first hypoxic episode to the third one. IL-10 (1 ng/ml) abolished these s[Ca²⁺]_i increases. Exposure of cultured hippocampal neurons with thapsigargin (1 渭M) or an inhibitor of phospholipase C (U73122, 1 渭M) for 10 min also abolished the s[Ca²⁺]_i increases. On the other hand, antagonist of ryanodine receptors (ryanodine, 1 渭M) did not affect this Ca²⁺ response. These studies appear to provide the first evidence that Ca²⁺ release from internal stores is affected by anti-inflammatory cytokine IL-10 in brain neurons. It is suggested that these data increase our understanding of the neuroprotective mechanisms of IL-10 in the early phase of hypoxia.