Sasakawa N, Nakaki T, Kakinuma E, Kato R
Department of Pharmacology, Keio University School of Medicine, Tokyo, Japan.
Brain Res. 1993 Sep 24;623(1):155-60. doi: 10.1016/0006-8993(93)90023-g.
Effects of high K+ stimulation on inositol polyphosphate accumulations and intracellular free calcium concentration ([Ca2+]i) were investigated in cultured rat cerebellar granule cells. When the [3H]inositol-labelled cells were stimulated with KCl, concentration-dependent accumulations of [3H]Ins(1,4,5)P3, [3H]InsP5 and [3H]InsP6 were observed. Nifedipine (3 microM), a calcium channel antagonist, inhibited the high (KCl, 90 mM) K(+)-induced accumulations of these inositol polyphosphates. In Ca(2+)-depleted and EGTA-containing (0.1 mM) medium, the high K(+)-induced inositol polyphosphate accumulation were completely inhibited. Similar results were also observed in the case of [Ca2+]i. These results suggest that the rise in [Ca2+]i caused by activation of voltage-dependent calcium channels plays an important roles in the high K(+)-induced accumulation of [3H]Ins(1,4,5)P3, [3H]InsP5 and [3H]InsP6 in cultured rat cerebellar granule cells.
在培养的大鼠小脑颗粒细胞中研究了高钾刺激对肌醇多磷酸积累和细胞内游离钙浓度（[Ca2+]i）的影响。当用氯化钾刺激[3H]肌醇标记的细胞时，观察到[3H]Ins(1,4,5)P3、[3H]InsP5和[3H]InsP6的浓度依赖性积累。钙通道拮抗剂硝苯地平（3 microM）抑制了高（氯化钾，90 mM）钾诱导的这些肌醇多磷酸的积累。在缺钙且含有EGTA（0.1 mM）的培养基中，高钾诱导的肌醇多磷酸积累被完全抑制。在[Ca2+]i的情况中也观察到了类似结果。这些结果表明，电压依赖性钙通道激活引起的[Ca2+]i升高在培养的大鼠小脑颗粒细胞中高钾诱导的[3H]Ins(1,4,5)P3、[3H]InsP5和[3H]InsP6积累中起重要作用。
