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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Neocortical GABA release at high intracellular sodium and low extracellular calcium: an anti-seizure mechanism
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Neocortical GABA release at high intracellular sodium and low extracellular calcium: an anti-seizure mechanism

机译：高细胞内钠和低细胞外钙释放新皮质GABA：抗癫痫发作机制

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摘要

In epilepsy, the GABA and glutamate balance may be disrupted and a transient decrease in extracellular calcium occurs before and during a seizure. Flow Cytometry based fluorescence activated particle sorting experiments quantified synaptosomes from human neocortical tissue, from both epileptic and non-epileptic patients (27.7% vs. 36.9% GABAergic synaptosomes, respectively). Transporter-mediated release of GABA in human and rat neocortical synaptosomes was measured using the superfusion technique for the measurement of endogenous GABA. GABA release was evoked by either a sodium channel activator or a sodium/potassium-ATPase inhibitor when exocytosis was possible or prevented, and when the sodium/calcium exchanger was active or inhibited. The transporter-mediated release of GABA is because of elevated intracellular sodium. A reduction in the extracellular calcium increased this release (in both non-epileptic and epileptic, except Rasmussen encephalitis, synaptosomes). The inverse was seen during calcium doubling. In humans, GABA release was not affected by exocytosis inhibition, that is, it was solely transporter-mediated. However, in rat synaptosomes, an increase in GABA release at zero calcium was only exhibited when the exocytosis was prevented. The absence of calcium amplified the sodium/calcium exchanger activity, leading to elevated intracellular sodium, which, together with the stimulation-evoked intracellular sodium increment, enhanced GABA transporter reversal. Sodium/calcium exchange inhibitors diminished GABA release. Thus, an important seizure-induced extracellular calcium reduction might trigger a transporter- and sodium/calcium exchanger-related anti-seizure mechanism by augmenting transporter-mediated GABA release, a mechanism absent in rats. Uniquely, the additional increase in GABA release because of calcium-withdrawal dwindled during the course of illness in Rasmussen encephalitis.
机译：在癫痫病中，癫痫发作之前和之中，GABA和谷氨酸的平衡可能会被破坏，并且细胞外钙的瞬时减少会发生。基于流式细胞术的荧光激活颗粒分选实验对来自癫痫病患者和非癫痫病患者的人新皮层组织的突触小体进行了定量分析（分别为27.7％和36.9％的GABA能突触小体）。使用超融合技术测量人和大鼠新皮层突触小体中转运蛋白介导的GABA释放，以测量内源性GABA。当可能或阻止胞吐作用时，或当钠/钙交换剂活跃或被抑制时，钠通道激活剂或钠/钾-ATP酶抑制剂可引起GABA释放。转运蛋白介导的GABA释放是由于细胞内钠升高。细胞外钙的减少增加了这种释放（在非癫痫和癫痫中，除了拉斯穆森脑炎，突触小体）。在钙加倍期间看到相反的现象。在人类中，GABA释放不受胞吐作用抑制的影响，也就是说，它仅是转运蛋白介导的。但是，在大鼠突触小体中，只有在防止胞吐作用时，钙在零钙下GABA的释放才会增加。钙的缺乏放大了钠/钙交换剂的活性，导致细胞内钠升高，再加上刺激引起的细胞内钠增量，增强了GABA转运蛋白的逆转。钠/钙交换抑制剂减少了GABA的释放。因此，重要的癫痫发作诱导的细胞外钙减少可能通过增加转运蛋白介导的GABA释放而触发了与转运蛋白和钠/钙交换剂相关的抗癫痫发作机制，而在大鼠中这种机制不存在。独特的是，在拉斯穆森脑炎的发病过程中，由于钙的吸收而导致的GABA释放量的增加有所减少。

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