Hertz L, Bender A S, Woodbury D M, White H S
Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
J Neurosci Res. 1989 Feb;22(2):209-15. doi: 10.1002/jnr.490220215.
Elevation of the extracellular potassium concentration above its "resting" level of 5.4 mM stimulated uptake of 45Ca2+ in primary cultures of astrocytes. This effect was only observed when cells were exposed to excess potassium shortly after their exposure to 45Ca2+ and was potently inhibited (IC50 congruent to 3 nM) by the calcium channel blocker nimodipine. In contrast, nimodipine exerted little effect on unstimulated basal uptake of 45Ca2+. These findings suggest that the therapeutic benefit of calcium channel blockers in epilepsy may result in part from the ability of these drugs to prevent calcium entry into astrocytes during seizures when the extracellular potassium is elevated four- to fivefold above normal.
细胞外钾离子浓度升高至高于其“静息”水平5.4 mM时，可刺激星形胶质细胞原代培养物对45Ca2+的摄取。只有当细胞在暴露于45Ca2+后不久就暴露于过量钾时，才会观察到这种效应，并且钙通道阻滞剂尼莫地平可有效抑制该效应（半数抑制浓度约为3 nM）。相比之下，尼莫地平对未受刺激的45Ca2+基础摄取几乎没有影响。这些发现表明，钙通道阻滞剂在癫痫治疗中的益处可能部分源于这些药物在癫痫发作期间细胞外钾离子浓度比正常水平升高四至五倍时，能够防止钙进入星形胶质细胞的能力。
