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Insulin inhibits voltage-dependent calcium influx into rod photoreceptors.

机译:胰岛素抑制依赖电压的钙流入棒状光感受器。

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Insulin inhibits the ERG b-wave and modulates L-type calcium currents (I(Ca)) in various preparations. We therefore examined insulin's effects on I(Ca) and depolarization-evoked [Ca2+]i increases in rod photoreceptors. Insulin inhibited I(Ca) and caused a dose-dependent reduction in the depolarization-evoked Ca2+ influx with an EC50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100 nM) and genistein (10 microM), prevented insulin from reducing the depolarization-evoked Ca2+ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptor-specific tyrosine kinase inhibitor, HNMPA-(AM)3 (50 microM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca2+ increase in rods. The results suggest that insulin inhibits Ca2+ influx through voltage-dependent I(Ca) in rod photoreceptors via tyrosine kinase activity.
机译:在各种制剂中,胰岛素抑制ERG的b波并调节L型钙电流(I(Ca))。因此,我们检查了胰岛素对棒状光感受器中I(Ca)和去极化诱发的[Ca2 +] i增加的影响。胰岛素抑制I(Ca)并引起去极化引起的Ca2 +内流的剂量依赖性降低,EC50为2.1 nM。酪氨酸激酶抑制剂lavendustin A(100 nM)和染料木黄酮(10 microM)阻止胰岛素减少杆中去极化引起的Ca2 +增加。它们活性较低的类似物,薰衣草素B和黄豆苷元具有相似的作用。胰岛素受体特异性酪氨酸激酶抑制剂HNMPA-(AM)3(50 microM)阻止胰岛素(30 nM)减少杆中去极化引起的Ca2 +增加。结果表明,胰岛素通过酪氨酸激酶活性通过杆状感光细胞中的电压依赖性I(Ca)抑制Ca2 +内流。

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