Ca2+ Buffering Capacity of Mitochondria After Oxygen-Glucose Deprivation in Hippocampal Neurons
Ca2+ Buffering Capacity of Mitochondria After Oxygen-Glucose Deprivation in Hippocampal Neurons
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DOI：
10.1007/s11064-008-9753-2
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发表时间：
2009-02
影响因子：
4.4
通讯作者：
Kensuke Tanaka;T. Iijima;T. Mishima;Kei Suga;K. Akagawa;Y. Iwao
中科院分区：
文献类型：
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作者：
Kensuke Tanaka;T. Iijima;T. Mishima;Kei Suga;K. Akagawa;Y. Iwao
在早期的一项研究中，我们发现线粒体在短时间的缺氧-葡萄糖剥夺(OGD)后超极化，这种反应似乎与随后的细胞凋亡或生存有关。在这里，我们证明了短时间OGD(30min；30OGD组)后的超极化增加了线粒体细胞内钙([Ca+]c)的缓冲能力。培养的大鼠海马神经元在不同时间(0、30、120分钟)分别给予谷氨酸处理后，引起钙离子内流。[Ca~(2+)]_c显著升高，线粒体[Ca~(2+)]_m迅速升高，[Ca~(2+)]_m升高，[Ca~(2+)]_c降低。达到峰值后，30OGD组较对照组[Ca~(2+)]_c下降更快。这种缓冲反应在30OGD组明显，而在120OGD组则不明显。线粒体缓冲能力的增强可能与短期缺血发作后的预适应有关。
In an earlier study, we showed that mitochondria hyperpolarized after short periods of oxygen-glucose deprivation (OGD), and this response appeared to be associated with subsequent apoptosis or survival. Here, we demonstrated that hyperpolarization following short periods of OGD (30 min; 30OGD group) increased the cytosolic Ca2+([Ca2+]c) buffering capacity in mitochondria. After graded OGD (0 min (control), 30 min, 120 min), rat cultured hippocampal neurons were exposed to glutamate, evoking Ca2+influx. The [Ca2+]clevel increased sharply, followed by a rapid increase in mitochondrial Ca2+[Ca2+]m. The increase in the [Ca2+]mlevel accompanied a reduction in the [Ca2+]clevel. After reaching a peak, the [Ca2+]clevel decreased more rapidly in the 30OGD group than in the control group. This buffering reaction was pronounced in the 30OGD group, but not in the 120OGD group. The enhanced buffering capacity of the mitochondria may be linked to preconditioning after short-term ischemic episodes.