Potassium depolarization of mammalian vestibular sensory cells increases [Ca 2+ ] i through voltage‐sensitive calcium channels

The existence of voltage‐sensitive Ca 2+ channels in type I vestibular hair cells of mammals has not been conclusively proven. Furthermore, Ca 2+ channels present in type II vestibular hair cells of mammals have not been pharmacologically identified. Fura‐2 fluorescence was used to estimate, in both cell types, intracellular Ca 2+ concentration ([Ca 2+ ] i ) variations induced by K + depolarization and modified by specific Ca 2+ channel agonists and antagonists. At rest, [Ca 2+ ] i was 90 ± 20 n m in both cell types. Microperifusion of high‐K + solution (50 m m ) for 1 s increased [Ca 2+ ] i to 290 ± 50 n m in type I ( n = 20) and to 440 ± 50 n m in type II cells ( n = 10). In Ca 2+ ‐free medium, K + did not alter [Ca 2+ ] i . The specific L‐type Ca 2+ channel agonist, Bay K, and antagonist, nitrendipine, modified in a dose‐dependent manner the K + ‐induced [Ca 2+ ] i increase in both cell types with maximum effect at 2 μ m and 400 n m , respectively. Ni 2+ , a T‐type Ca 2+ channel blocker, reduced K + ‐evoked Ca 2+ responses in a dose‐dependent manner. For elevated Ni 2+ concentrations, the response was differently affected by Ni 2+ alone, or combined to nitrendipine (500 n m ). In optimal conditions, nitrendipine and Ni 2+ strongly depressed by 95% the [Ca 2+ ] i increases. By contrast, neither ω‐agatoxin IVA (1 μ m ), a specific P‐ and Q‐type blocker, nor ω‐conotoxin GVIA (1 μ m ), a specific N‐type blocker, affected K + ‐evoked Ca 2+ i responses. These results provide the first direct evidence that L‐ and probably T‐type channels control the K + ‐induced Ca 2+ influx in both types of sensory cells.