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Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells
by
Ohtubo Yoshitaka
in
Channel gating
/ Firing rate
/ Gene expression
/ Inositol
/ Inositol 1,4,5-trisphosphate receptors
/ Neurotransmitter release
/ Physiology
/ Polymerase chain reaction
/ Signal transduction
/ Sodium channels
/ Sodium channels (voltage-gated)
/ Software
/ Taste receptor neurons
/ Tetrodotoxin
2021
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Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells
by
Ohtubo Yoshitaka
in
Channel gating
/ Firing rate
/ Gene expression
/ Inositol
/ Inositol 1,4,5-trisphosphate receptors
/ Neurotransmitter release
/ Physiology
/ Polymerase chain reaction
/ Signal transduction
/ Sodium channels
/ Sodium channels (voltage-gated)
/ Software
/ Taste receptor neurons
/ Tetrodotoxin
2021
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
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Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells
by
Ohtubo Yoshitaka
in
Channel gating
/ Firing rate
/ Gene expression
/ Inositol
/ Inositol 1,4,5-trisphosphate receptors
/ Neurotransmitter release
/ Physiology
/ Polymerase chain reaction
/ Signal transduction
/ Sodium channels
/ Sodium channels (voltage-gated)
/ Software
/ Taste receptor neurons
/ Tetrodotoxin
2021
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Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells
Journal Article
Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells
2021
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Overview
Action potentials play an important role in neurotransmitter release in response to taste. Here, I have investigated voltage-gated Na+ channels, a primary component of action potentials, in respective cell types of mouse fungiform taste bud cells (TBCs) with in situ whole-cell clamping and single-cell RT-PCR techniques. The cell types of TBCs electrophysiologically examined were determined immunohistochemically using the type III inositol 1,4,5-triphoshate receptor as a type II cell marker and synaptosomal-associated protein 25 as a type III cell marker. I show that type II cells, type III cells, and TBCs not immunoreactive to these markers (likely type I cells) generate voltage-gated Na+ currents. The recovery following inactivation of these currents was well fitted with double exponential curves. The time constants in type III cells (~20 ms and ~ 1 s) were significantly slower than respective time constants in other cell types. RT-PCR analysis indicated the expression of Nav1.3, Nav1.5, Nav1.6, and β1 subunit mRNAs in TBCs. Pharmacological inhibition and single-cell RT-PCR studies demonstrated that type II and type III cells principally express tetrodotoxin (TTX)-sensitive Nav1.3 channels and that ~ 30% of type I cells express TTX-resistant Nav1.5 channels. The auxiliary β1 subunit that modulates gating kinetics was rarely detected in TBCs. As the β1 subunit co-expressed with an α subunit is known to accelerate the recovery from inactivation, it is likely that voltage-gated Na+ channels in TBCs may function without β subunits. Slow recovery from inactivation, especially in type III cells, may limit high-frequency firing in response to taste substances.
Publisher
Springer Nature B.V
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