Insulin inhibits the ERG b-wave and modulates L-type calcium currents (ICa) in various preparations. We therefore examined insulin's effects on ICa and depolarization-evoked [Ca2+]i increases in rod photoreceptors. Insulin inhibited ICa and caused a dose-dependent reduction in the depolarization-evoked Ca2+ influx with an EC50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100nM) and genistein (10μM), 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 (50μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca2+ increase in rods. The results suggest that insulin inhibits Ca2+ influx through voltage-dependent ICa in rod photoreceptors via tyrosine kinase activity.
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