title: Potassium depolarization of mammalian vestibular sensory cells increases [Ca2+]i through voltage-sensitive calcium channels.
abstract: The existence of voltage-sensitive Ca2+ channels in type I vestibular hair cells of mammals has not been conclusively proven. Furthermore, Ca2+ 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 Ca2+ concentration ([Ca2+]i) variations induced by K+ depolarization and modified by specific Ca2+ channel agonists and antagonists. At rest, [Ca2+]i was 90 +/- 20 nM in both cell types. Microperifusion of high-K+ solution (50 mM) for 1 s increased [Ca2+]i to 290 +/- 50 nM in type I (n = 20) and to 440 +/- 50 nM in type II cells (n = 10). In Ca2+-free medium, K+ did not alter [Ca2+]i. The specific L-type Ca2+ channel agonist, Bay K, and antagonist, nitrendipine, modified in a dose-dependent manner the K+-induced [Ca2+]i increase in both cell types with maximum effect at 2 microM and 400 nM, respectively. Ni2+, a T-type Ca2+ channel blocker, reduced K+-evoked Ca2+ responses in a dose-dependent manner. For elevated Ni2+ concentrations, the response was differently affected by Ni2+ alone, or combined to nitrendipine (500 nM). In optimal conditions, nitrendipine and Ni2+ strongly depressed by 95% the [Ca2+]i increases. By contrast, neither omega-agatoxin IVA (1 microM), a specific P- and Q-type blocker, nor omega-conotoxin GVIA (1 microM), a specific N-type blocker, affected K+-evoked Ca2+i responses. These results provide the first direct evidence that L- and probably T-type channels control the K+-induced Ca2+ influx in both types of sensory cells.
authors.affiliation: INSERM U-432, Neurobiologie et Développement du système vestibulaire, Université Montpellier II, France. catboyer@crit.univ-montp2.fr
authors.forename: C
authors.initials: C
authors.lastname: Boyer
authors.forename: J
authors.initials: J
authors.lastname: Lehouelleur
authors.forename: A
authors.initials: A
authors.lastname: Sans
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D004594:Electrophysiology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects*; D011188:Potassium / Q000494:pharmacology*; D014722:Vestibule, Labyrinth / Q000166:cytology / Q000187:drug effects / Q000502:physiology*
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D011188:Potassium; D002118:Calcium