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1The Bobby R. Alford Department of Otorhinolaryngology and Communicative Sciences, Baylor College of Medicine, Houston, Texas 77030; and 2Department of Neurobiology, Pharmacology, and Physiology, University of Chicago, Chicago, Illinois 60637
Submitted 3 April 2002; accepted in final form 13 March 2003
When studied in vitro, type I hair cells in amniote vestibular organs have
a large, negatively activating K+ conductance. In type II hair
cells, as in nonvestibular hair cells, outwardly rectifying K+
conductances are smaller and more positively activating. As a result, type I
cells have more negative resting potentials and smaller input resistances than
do type II cells; large inward currents fail to depolarize type I cells above
–60 mV. In nonvestibular hair cells, afferent transmission is mediated
by voltage-gated Ca2+ channels that activate positive to
–60 mV. We investigated whether Ca2+ channels in
type I cells activate more negatively so that quantal transmission can occur
near the reported resting potentials. We used the perforated patch method to
record Ca2+ channel currents from type I and type II
hair cells isolated from the rat anterior crista (postnatal days 4–20).
The activation range of the Ca2+ currents of type I hair
cells differed only slightly from that of type II cells or nonvestibular hair
cells. In 5 mM external Ca2+, currents in type I and
type II cells were half-maximal at –41.1 ± 0.5 (SE) mV
(n = 10) and –37.2 ± 0.2 mV (n = 10),
respectively. In physiological external Ca2+ (1.3 mM),
currents in type I cells were half-maximal at –46 ± 1 mV
(n = 8) and just 1% of maximal at –72 mV. These results lend
credence to suggestions that type I cells have more positive resting
potentials in vivo, possibly through K+ accumulation in the
synaptic cleft or inhibition of the large K+ conductance.
Ca2+ channel kinetics were also unremarkable; in both
type I and type II cells, the currents activated and deactivated rapidly and
inactivated only slowly and modestly even at large depolarizations. The
Ca2+ current included an L-type component with
relatively low sensitivity to dihydropyridine antagonists, consistent with the
subunit being CaV1.3 (1D). Rat vestibular
epithelia and ganglia were probed for L-type -subunit expression with
the reverse transcription-polymerase chain reaction. The epithelia expressed
CaV1.3 and the ganglia expressed CaV1.2
(1C).
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