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題 名 | Astrocytes Modulate Thapsigargin-induced Changes in Calcium Concentration and Neuronal Survival=神經膠細胞調控Thapsigargin對神經細胞的內鈣濃度及生存的作用 |
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作 者 | 姚智榮; 林啟萬; 蕭水銀; | 書刊名 | Proceedings of the National Science Council : Part B, Life Science |
卷 期 | 24:2 2000.04[民89.04] |
頁 次 | 頁81-87 |
分類號 | 364.67911 |
關鍵詞 | 神經膠細胞; 神經細胞; Cerebellar granule neurons; Thapsigargin; Astrocyte; Intracellular Ca[fec7]; Survival; |
語 文 | 英文(English) |
英文摘要 | When mature cerebellar granule neurons (CGN) grown in high K+ (25 mM K+, HK)-serum containing medium are subjected to the HK/serum deprivation, they are destined for neuronal death. In this study, we attempted to elucidate the roles of endoplasmic reticular (ER) Ca2+-store and co-cultured astrocytes in HK/serum deprivation induced neuronal death. Thapsigargin (TG), an inhibitor of ER Ca2+- ATPase was simultaneously applied with normal K+ (5 mM K+, NK) serum free medium, and its effects on neuronal death in either astrocyte-poor or astrocyte-rich culture were examined. By means of the fura-2 microfluorimetric technique, we monitored the changes of the intracellular Ca2+ concentration, [Ca2+]i, associated with neuronal death under various treatments. The results obtained showed that in astrocyte-poor cultures of mature CGN (10 days in vitro, DIV), the basal level of [Ca2+]i markedly decreased from 184 ?5 to 89.7 ?5 nM 24 h after HK/serum deprivation. Although treatment with TG slightly increased the [Ca2+]i to 117.6 ?4 nM, the survival rate of the neurons was even worse; it was reduced from 49 ?4% to 28 ?2%. In the astrocyte-rich cultures, HK/serum deprivation also caused a profound reduction of neuronal [Ca2+]i from 166 ?3 to 90.2 ?6 nM, accompanied by even more serious neuronal death (95.5 ?1%). On the other hand, treatment with TG in astrocyterich cultures further lowered the [Ca2+]i to 65 ?2 nM but markedly improved the neuronal survival rate from 4.5 ?1% to 60 ?2% in a concentration- dependent manner. The strong implication of these findings is that ER Ca2+-store and astrocytes participate in modulating the responses of neurons to stress stimulation. |
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