Reverse Operation of the Na+ ‐Ca2+ Exchanger Mediates Ca 2+ Influx during Anoxia in Mammalian CNS White Matter a

Reverse Operation of the Na+ ‐Ca2+ Exchanger Mediates Ca 2+ Influx during Anoxia in Mammalian CNS White Matter a
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Na+ ‐Ca2+ 交换器的反向操作介导哺乳动物中枢神经系统白质缺氧期间 Ca 2+ 流入

DOI:
10.1111/j.1749-6632.1991.tb17321.x
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发表时间:
1991
影响因子:
5.2
通讯作者:
B. Ransom
B. Ransom
中科院分区:
综合性期刊3区
文献类型:
--
作者:
P. Stys;S. Waxman;B. Ransom

文献摘要

被引文献

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哺乳动物中枢神经系统(CNS)中的中枢白质束(WM),如皮质下通路和脊髓束,在缺氧/缺血后会遭受不可逆的损伤,对中枢神经系统的功能完整性至关重要。缺氧诱导的细胞死亡似乎是由细胞内CaZf的持续增加引起的。在灰质中,缺氧时Ca2+内流进入细胞质被认为是通过nmdar受体控制的。具体来说,细胞外Ca2+进入细胞质室的关键步骤尚不清楚。我们利用体外大鼠视神经(CNS WM束的一个代表)研究了这个问题。我们的研究结果表明,在WM缺氧期间发生的破坏性CaZ+内流的很大一部分是由Na+-Ca2+交换器介导的,由于Na+通过电压门控Naf通道内流而被迫以相反模式运行。
Central white matter (WM) tracts in the mammalian central nervous system (CNS), such as subcortical pathways and spinal cord tracts that are critical to the functional integrity of the CNS, suffer irreversible injury after anoxia/ischemia. Anoxia-induced cell death appears to be caused by sustained increases in intracellular CaZf. In gray matter, Ca2+ influx into the cytoplasm during anoxia is thought to occur via NMDAreceptor-gated The mechanisms of anoxic injury in CNS WM are less well understood; specifically, the critical step by which extracellular Ca2+ enters the cytoplasmic compartment is not known. We have studied this question using the in vitro rat optic nerve, a representative CNS WM tract. Our results indicate that a large part of the damaging CaZ+ influx that occurs during anoxia in WM is mediated by the Na+-Ca2+ exchanger, forced to operate in the reverse mode due to Na+ influx via voltage-gated Naf channels.