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Potassium depolarization of mammalian vestibular sensory cells increases [Ca2+]i through voltage-sensitive calcium channels.

Authors :
Boyer C
Lehouelleur J
Sans A
Source :
The European journal of neuroscience [Eur J Neurosci] 1998 Mar; Vol. 10 (3), pp. 971-5.
Publication Year :
1998

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.

Details

Language :
English
ISSN :
0953-816X
Volume :
10
Issue :
3
Database :
MEDLINE
Journal :
The European journal of neuroscience
Publication Type :
Academic Journal
Accession number :
9753164
Full Text :
https://doi.org/10.1046/j.1460-9568.1998.00107.x