Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Biophys J
2004 Dec 01;876:3862-72. doi: 10.1529/biophysj.104.045963.
Show Gene links
Show Anatomy links
Use-dependent potentiation of the Nav1.6 sodium channel.
Zhou W
,
Goldin AL
.
???displayArticle.abstract??? Nav1.2 and Nav1.6 are two voltage-gated sodium channel isoforms that are abundant in the adult central nervous system. These channels are expressed in different cells and localized in different neuronal regions, which may reflect functional specialization. To examine this possibility, we compared the properties of Nav1.2 and Nav1.6 in response to a rapid series of repetitive depolarizations. Currents through Nav1.6 coexpressed with beta1 demonstrated use-dependent potentiation during a rapid train of depolarizations. This potentiation was in contrast to the use-dependent decrease in current for Nav1.2 with beta1. The voltage dependence of potentiation correlated with the voltage dependence of activation, and it still occurred when fast inactivation was removed by mutation. Rapid stimulation accelerated a slow phase of activation in the Nav1.6 channel that had fast inactivation removed, resulting in faster channel activation. Although the Nav1.2 channel with fast inactivation removed also demonstrated slightly faster activation, that channel showed very pronounced slow inactivation compared to Nav1.6. These results indicate that potentiation of Nav1.6 sodium currents results from faster channel activation, and that this effect is masked by slow inactivation in Nav1.2. The data suggest that Nav1.6 might be more resistant to inactivation, which might be helpful for high-frequency firing at nodes of Ranvier compared to Nav1.2.
Aldrich,
A reinterpretation of mammalian sodium channel gating based on single channel recording.
, Pubmed
Aldrich,
A reinterpretation of mammalian sodium channel gating based on single channel recording.
,
Pubmed
Armstrong,
Fast and slow steps in the activation of sodium channels.
1979,
Pubmed
Boiko,
Compact myelin dictates the differential targeting of two sodium channel isoforms in the same axon.
2001,
Pubmed
Caldwell,
Sodium channel Na(v)1.6 is localized at nodes of ranvier, dendrites, and synapses.
2000,
Pubmed
Catterall,
From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels.
2000,
Pubmed
Colbert,
Slow recovery from inactivation of Na+ channels underlies the activity-dependent attenuation of dendritic action potentials in hippocampal CA1 pyramidal neurons.
1997,
Pubmed
Goldin,
Nomenclature of voltage-gated sodium channels.
2000,
Pubmed
Goldin,
Resurgence of sodium channel research.
2001,
Pubmed
Goldin,
Evolution of voltage-gated Na(+) channels.
2002,
Pubmed
Goldin,
Expression of ion channels by injection of mRNA into Xenopus oocytes.
1991,
Pubmed
,
Xenbase
Kaplan,
Differential control of clustering of the sodium channels Na(v)1.2 and Na(v)1.6 at developing CNS nodes of Ranvier.
2001,
Pubmed
Keynes,
On the slowly rising phase of the sodium gating current in the squid giant axon.
1998,
Pubmed
Litt,
Localization of a human brain sodium channel gene (SCN2A) to chromosome 2.
1989,
Pubmed
Malo,
Three brain sodium channel alpha-subunit genes are clustered on the proximal segment of mouse chromosome 2.
1991,
Pubmed
Malo,
Localization of a putative human brain sodium channel gene (SCN1A) to chromosome band 2q24.
1994,
Pubmed
Plummer,
Exon organization, coding sequence, physical mapping, and polymorphic intragenic markers for the human neuronal sodium channel gene SCN8A.
1998,
Pubmed
Pugsley,
Effects of bisaramil, a novel class I antiarrhythmic agent, on heart, skeletal muscle and brain Na+ channels.
1998,
Pubmed
,
Xenbase
Smith,
Functional analysis of the rat I sodium channel in xenopus oocytes.
1998,
Pubmed
,
Xenbase
Smith,
Functional analysis of the mouse Scn8a sodium channel.
1998,
Pubmed
,
Xenbase
Spampanato,
Functional effects of two voltage-gated sodium channel mutations that cause generalized epilepsy with febrile seizures plus type 2.
2001,
Pubmed
,
Xenbase
Vandenberg,
A sodium channel gating model based on single channel, macroscopic ionic, and gating currents in the squid giant axon.
1991,
Pubmed
West,
A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.
1992,
Pubmed
,
Xenbase
