voltage-gated sodium channels

'voltage-gated sodium channels' can also refer to...

voltage-gated sodium channels

Voltage-gated sodium channels

Voltage-gated sodium channels

Neurological perspectives on voltage-gated sodium channels

Hereditary dysfunction of voltage-gated sodium channels: from clinical phenotype to molecular mechanisms

Calcium-dependent regulation of voltage-gated sodium channels in cardiac myocytes: just the beginning?

Intracellular calcium modulation of voltage-gated sodium channels in ventricular myocytes

Mechanisms of (local) anaesthetics on voltage‐gated sodium and other ion channels

Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels?

Voltage-gated sodium channel mutations and painful neuropathy: Nav1.9 joins the family

Pacemaker, potassium, calcium, sodium: stretch modulation of the voltage-gated channels

Differential Evolution of Voltage-Gated Sodium Channels in Tetrapods and Teleost Fishes

Seizure suppression through manipulating splicing of a voltage-gated sodium channel

Hereditary dysfunction of voltage-gated sodium channels: from clinical phenotype to molecular mechanisms

Identification of Novel Voltage-Gated Sodium Channel Mutations in Human Head and Body Lice (Phthiraptera: Pediculidae)

The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy

Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice

Parallel Evolution of Tetrodotoxin Resistance in Three Voltage-Gated Sodium Channel Genes in the Garter Snake Thamnophis sirtalis

Detection of Knockdown Resistance Mutations in Anopheles sacharovi (Diptera: Culicidae) and Genetic Distance with Anopheles gambiae (Diptera: Culicidae) Using cDNA Sequencing of the Voltage-Gated Sodium Channel Gene


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A family of multisubunit ion channels with an aqueous pore ~0.4 nm diameter formed by the α subunits, with a negatively charged interior that inhibits the passage of anions. The various β subunits confer different responsiveness on channels, according to the tissue. The channel is responsible for electrical excitability of neurons, and a small depolarization of the cell (usually caused by an approaching action potential), triggers the channel to open. Within a millisecond ~1000 sodium ions pass through before the channel spontaneously closes. The channel is then refractory until the membrane potential approaches the resting potential. There are around 100 channels/μm2 in unmyelinated axons, but in myelinated axons they are concentrated at the nodes of Ranvier. Mutations in either the α or β subunits of the neuronal NaV1.1 (SCN1A and B) cause various forms of epilepsy. NaV1.2 (SCN2A) is similar to NaV1.1 but found in caudal regions of the brain; mutations cause febrile seizures. NaV1.3 is also found in the central nervous system. NaV1.4 (SCN4A and -B) is the skeletal muscle form and mutations in the gene are involved in various muscular disorders, including hyperkalemic periodic paralysis, myotonia, and hypokalemic periodic paralysis; mutations in SCN4B cause long QT syndrome-10. NaV1.5 is expressed in the heart, brain, and gastrointestinal tract, and mutations in the gene SCN5A cause long QT syndrome-3 and Brugada syndrome-1. NaV1.6 (alpha subunit encoded by SCN8A) may be defective in hereditary neurodegenerative diseases. SCN7A (previously SCN6A) is thought to be the sodium-level sensor in the brain. Mutations in SCN9A (alpha subunit of NaV1.7), the major sodium channel expressed in bronchial and arterial smooth muscle, cause primary erythromelalgia, congenital insensitivity to pain, and paroxysmal extreme pain disorder. NaV1.8 (SCN10A) is specific to peripheral sensory neurons. NaV1.9 (SCN11A) mediates brain-derived neurotrophic factor-evoked membrane depolarization through the receptor tyrosine kinase NTRK2 and is implicated in inflammatory but not acute pain. Many toxins (see anthopleurins; batrachotoxins; brevetoxins; calitoxins; ciguatoxins; conotoxins; jingzhaotoxin-III; saxitoxin; scorpion toxins; tetrodotoxin; veratridine) affect the channel with serious consequences. Compare amiloride-sensitive sodium channels.

Subjects: Medicine and Health.

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