Astrocytic regulation of the recovery of extracellular potassium after seizures in vivo
Astrocytic regulation of the recovery of extracellular potassium after seizures in vivo
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DOI：
10.1046/j.1460-9568.1999.00587.x
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发表时间：
1999-05-01
影响因子：
3.4
通讯作者：
Stringer, JL
中科院分区：
文献类型：
--
作者：
Xiong, ZQ;Stringer, JL
神经胶质细胞被认为在细胞外钾浓度（[K+]（o））的调节中起主要作用，特别是当[K+]（o）增加时。使用离子选择性电极，我们比较了[K+]（o）的变化，在反应性星形胶质细胞的存在下，神经胶质细胞的功能减少后，在海马麻醉的成年大鼠的齿状回。用20 Hz刺激角束诱发癫痫发作时和发作后，通过测定[K+]（o）的上限水平和[K+]（o）的半数恢复时间来确定齿状回[K +]（o）的调节。反应性星形胶质细胞诱导反复癫痫发作，其存在被证实了胶质细胞酸性蛋白（GFAP）和波形蛋白免疫反应性的定性增加。为了抑制胶质细胞功能，将可逆代谢抑制剂氟柠檬酸（FC）或不可逆毒素α-氨基己二酸（α-AA）注射到齿状回区域，并分别在8 h或2 d后监测[K+]（o）的调节。使用α-氨基己二酸后，GFAP染色消失，证明了齿状回中星形胶质细胞的消失。与对照动物相比，在存在反应性星形胶质细胞的情况下，癫痫发作期间的峰值[K+]（o）或癫痫发作后[K+]（o）的恢复半衰期无显著变化，α-氨基己二酸盐显著减慢[K+]（o）的恢复速率，但未改变上限[K+]（o）。氟柠檬酸可逆地降低[K+]（o）上限，但也减慢[K+]（o）的恢复速率。总体而言，我们的研究结果表明，正常的胶质细胞功能是需要在体内癫痫发作后恢复升高的[K+]（o）。
Glial cells are believed to play a major role in the regulation of the extracellular potassium concentration ([K+](o)), particularly when the [K+](o) is increased. Using ion-selective electrodes, we compared the [K+](o) changes in the dentate gyrus of urethane-anaesthetized adult rats in the presence of reactive astrocytes and after reduction of glial function. The regulation of [K+](o) in the dentate gyrus was determined by measuring the ceiling level of [K+](o) and the half-time of recovery of [K+](o) during and after seizures produced by 20 Hz trains of stimulation to the angular bundle. Reactive astrocytes were induced by repeated seizures and their presence was confirmed by a qualitative increase in glial fibrillary acidic protein (GFAP) and vimentin immunoreactivity. To inhibit glial function, fluorocitrate (FC), a reversible metabolic inhibitor, or alpha-aminoadipate (alpha-AA), an irreversible toxin, was injected into the dentate gyrus region, and the regulation of [K+](o) was monitored for 8 h or 2 days later, respectively. After alpha-aminoadipate, loss of astrocytes in the dentate gyrus was demonstrated by loss of staining for GFAP. In the presence of reactive astrocytes there was no significant change in the peak [K+](o) during seizures or the half-time of recovery of [K+](o) after seizures compared to control animals, alpha-Aminoadipate significantly slowed the rate of recovery of [K+](o), but did not change the ceiling [K+](o). Fluorocitrate reversibly decreased the ceiling [K+](o), but also slowed the rate of recovery of [K+](o). Overall our results suggest that normal glial function is required for the recovery of elevated [K+](o) after seizures in vivo.