Ca2+ signaling in gerbil CA3 hippocampal neurons following transient in vivo ischemia.
Ca2+ signaling in gerbil CA3 hippocampal neurons following transient in vivo ischemia.
复制标题
短暂体内缺血后沙鼠 CA3 海马神经元中的 Ca2 信号传导。
DOI：
10.1016/s0304-3940(00)01094-6
复制
发表时间：
2000
影响因子：
2.5
通讯作者：
Connor,JA
中科院分区：
文献类型：
--
作者：
Shuttleworth,CW;Greenwood,AC;Connor,JA
使用海马CA 1区中缺血后神经元死亡的沙鼠模型，最近显示在缺血损伤后2天检查的神经元中电压门控Ca 2+内流存在强烈的下调（康纳，J.A.，Razani-Boroujerdi，S.，格林伍德，AC，Corpus，R.J.，Petrozzino，J.J.和Lin，R.C.，沙土鼠短暂缺血后CA 1神经元中电压依赖性Ca 2+信号传导减少，神经生理学杂志，81（1999）299-306）。本研究的目的是确定是否有类似的变化发生在锥体神经元的CA 3区，相对耐短暂性缺血。在体外细胞内记录和荧光Ca 2+测量从冠状切片中的CA 3神经元制备的控制和1或2天后，在体内缺血。在控制和缺血后动物的切片中，CA 3神经元的电生理特性与显著的电压门控性Ca 2+内流一致，导致尖峰频率适应。定量结果表明，动作电位序列诱发的Ca 2+瞬变无显着差异。将该Ca 2+信号传导与来自相同制剂的CA 1神经元中的反应进行比较，其显示在缺血后2天显著减少的Ca 2+内流。这些发现表明，减少钙离子信号不是一个普遍的特点，锥体神经元缺血后，但注定要死的神经元的特征。
Using the gerbil model of post-ischemic neuron death in the hippocampal CA1 region, it was recently shown that there is a strong down-regulation of voltage-gated Ca2+influx in neurons examined at 2 days after the ischemic insult (Connor, J.A., Razani-Boroujerdi, S., Greenwood, A.C., Cormier, R.J., Petrozzino, J.J. and Lin, R.C., Reduced voltage-dependent Ca2+signaling in CA1 neurons after brief ischemia in gerbils, J. Neurophysiol., 81 (1999) 299–306). The aim of the present study was to determine whether a similar change occurs in pyramidal neurons of the CA3 region that are relatively resistant to transient ischemia. In vitro intracellular recordings and fluorometric Ca2+measurements were made from CA3 neurons in coronal slices prepared from controls and 1 or 2 days following in vivo ischemia. In slices from control and post-ischemic animals, the electrophysiological properties of CA3 neurons were consistent with significant voltage-gated Ca2+influx, leading to spike frequency adaptation. Quantitative results indicated no significant difference in Ca2+transients evoked by action potential trains. This Ca2+signaling was compared with responses in CA1 neurons from the same preparations, which showed substantially diminished Ca2+influx at 2 days post-ischemia. These findings suggest that diminished Ca2+-signaling is not a general feature of pyramidal neurons following ischemia, but is characteristic of neurons destined to die.