Abstract
The voltage-gated sodium channel Na(V)1.7 is preferentially expressed in peripheral somatic and visceral sensory neurons, olfactory sensory neurons and sympathetic ganglion neurons. Na(V)1.7 accumulates at nerve fibre endings and amplifies small subthreshold depolarizations, poising it to act as a threshold channel that regulates excitability. Genetic and functional studies have added to the evidence that Na(V)1.7 is a major contributor to pain signalling in humans, and homology modelling based on crystal structures of ion channels suggests an atomic-level structural basis for the altered gating of mutant Na(V)1.7 that causes pain.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Biophysics
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Humans
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Models, Molecular
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Mutation / genetics
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NAV1.7 Voltage-Gated Sodium Channel / genetics*
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NAV1.7 Voltage-Gated Sodium Channel / metabolism*
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Pain* / genetics
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Pain* / pathology
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Pain* / physiopathology
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Peripheral Nerves / drug effects
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Peripheral Nerves / metabolism
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Peripheral Nerves / physiopathology
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Sodium Channel Blockers / pharmacology
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Tetrodotoxin / pharmacology
Substances
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NAV1.7 Voltage-Gated Sodium Channel
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SCN9A protein, human
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Sodium Channel Blockers
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Tetrodotoxin