Reduced voltage-dependent Ca2+ signaling in CA1 neurons after brief ischemia in gerbils.
Reduced voltage-dependent Ca2+ signaling in CA1 neurons after brief ischemia in gerbils.
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DOI：
10.1152/jn.1999.81.1.299
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发表时间：
1999
影响因子：
2.5
通讯作者：
John A. Connor;S. Razani-Boroujerdi;A. C. Greenwood;Robert J. Cormier;J. Petrozzino;Rick C. S. Lin
中科院分区：
文献类型：
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作者：
John A. Connor;S. Razani-Boroujerdi;A. C. Greenwood;Robert J. Cormier;J. Petrozzino;Rick C. S. Lin
细胞内Ca 2+的初始过载在短暂缺血后几天死亡的海马CA 1神经元的延迟死亡中起着关键作用。没有直接证据，流行的假设是，钙超载可能会复发，直到细胞死亡。在这里，我们报告的第一次测量的细胞内钙离子在脑切片制备1，2和3天后，短暂（5分钟）缺血的活CA 1神经元。由于没有持续Ca 2+超载的迹象，电压依赖性Ca 2+瞬变在再灌注2-3天后实际上减少。负荷后静息Ca ~（2+）水平和恢复率与未接受缺血损伤的神经元相似。河豚毒素不敏感的钙峰，通常由这些神经元产生的，是不存在的2天postisemia，是一个大部分的钙依赖性穗列车适应。这些令人惊讶的发现可能会导致迟发性神经元死亡和干预的新视角。
An initial overload of intracellular Ca2+ plays a critical role in the delayed death of hippocampal CA1 neurons that die a few days after transient ischemia. Without direct evidence, the prevailing hypothesis has been that Ca2+ overload may recur until cell death. Here, we report the first measurements of intracellular Ca2+ in living CA1 neurons within brain slices prepared 1, 2, and 3 days after transient (5 min) ischemia. With no sign of ongoing Ca2+ overload, voltage-dependent Ca2+ transients were actually reduced after 2-3 days of reperfusion. Resting Ca2+ levels and recovery rate after loading were similar to neurons receiving no ischemic insult. The tetrodotoxin-insensitive Ca spike, normally generated by these neurons, was absent at 2 days postischemia, as was a large fraction of Ca2+-dependent spike train adaptation. These surprising findings may lead to a new perspective on delayed neuronal death and intervention.