C. Boyer et al., POTASSIUM DEPOLARIZATION OF MAMMALIAN VESTIBULAR SENSORY CELLS INCREASES [CA2-SENSITIVE CALCIUM CHANNELS(](I) THROUGH VOLTAGE), European journal of neuroscience, 10(3), 1998, pp. 971-975
The existence of voltage-sensitive Ca2+ channels in type I vestibular
hair cells of mammals has not been conclusively proven. Furthermore, C
a2+ 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 a
t 2 mu M and 400 nM, respectively. Ni2+, a T-type Ca2+ channel blocker
, reduced K+-evoked Ca2+ responses in a dose-dependent manner. For ele
vated Ni2+ concentrations, the response was differently affected by Ni
2+ alone, or combined to nitrendipine (500 nM). In optimal conditions,
nitrendipine and Ni2+ strongly depressed by 95% the [Ca2+](i) increas
es. By contrast, neither omega-agatoxin IVA (1 mu M), a specific P- an
d Q-type blocker, nor omega-conotoxin GVIA (1 mu M), a specific N-type
blocker, affected K+-evoked Ca-i(2+) responses. These results provide
the first direct evidence that L- and probably T-type channels contro
l the K+-induced Ca2+ influx in both types of sensory cells.