Literature DB >> 7507618

Na+ currents that fail to inactivate.

C P Taylor1.   

Abstract

Textbook accounts give the impression that Na+ channels are short-acting binary switches: depolarization opens them, but only for about one millisecond. In contrast to this simplified view, a small but significant fraction of the total Na+ current in neurons occurs because channels open after long delays or in long-duration bursts of openings. Such non-inactivating Na+ current acts physiologically in neurons to amplify synaptic potentials and enhance endogenous rhythmicity, and also to aid repetitive firing of action potentials. In glial cells it also may regulate Na(+)-K+ ATPase activity. The evidence for non-inactivating Na+ current in a variety of neurons and glia is reviewed, along with a brief discussion of its ion channel substrate and its relevance for neurological diseases and drug therapy.

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Year:  1993        PMID: 7507618     DOI: 10.1016/0166-2236(93)90077-y

Source DB:  PubMed          Journal:  Trends Neurosci        ISSN: 0166-2236            Impact factor:   13.837


  34 in total

1.  High conductance sustained single-channel activity responsible for the low-threshold persistent Na(+) current in entorhinal cortex neurons.

Authors:  J Magistretti; D S Ragsdale; A Alonso
Journal:  J Neurosci       Date:  1999-09-01       Impact factor: 6.167

2.  Direct demonstration of persistent Na+ channel activity in dendritic processes of mammalian cortical neurones.

Authors:  J Magistretti; D S Ragsdale; A Alonso
Journal:  J Physiol       Date:  1999-12-15       Impact factor: 5.182

3.  Ionic mechanisms underlying repetitive high-frequency burst firing in supragranular cortical neurons.

Authors:  J C Brumberg; L G Nowak; D A McCormick
Journal:  J Neurosci       Date:  2000-07-01       Impact factor: 6.167

4.  Membrane stretch affects gating modes of a skeletal muscle sodium channel.

Authors:  I V Tabarean; P Juranka; C E Morris
Journal:  Biophys J       Date:  1999-08       Impact factor: 4.033

5.  Cytosolic Ca2+ changes during in vitro ischemia in rat hippocampal slices: major roles for glutamate and Na+-dependent Ca2+ release from mitochondria.

Authors:  Y Zhang; P Lipton
Journal:  J Neurosci       Date:  1999-05-01       Impact factor: 6.167

6.  Activation of synaptic NMDA receptors by action potential-dependent release of transmitter during hypoxia impairs recovery of synaptic transmission on reoxygenation.

Authors:  A M Sebastião; A de Mendonca; T Moreira; J A Ribeiro
Journal:  J Neurosci       Date:  2001-11-01       Impact factor: 6.167

Review 7.  Sodium channel toxins and neurotransmitter release.

Authors:  André Ricardo Massensini; Marco Aurélio Romano-Silva; Marcus Vinícius Gomez
Journal:  Neurochem Res       Date:  2003-10       Impact factor: 3.996

8.  Slow inactivation of Na+ current and slow cumulative spike adaptation in mouse and guinea-pig neocortical neurones in slices.

Authors:  I A Fleidervish; A Friedman; M J Gutnick
Journal:  J Physiol       Date:  1996-05-15       Impact factor: 5.182

9.  Scutellarin blocks sodium current in freshly isolated mouse hippocampal CA1 neurons.

Authors:  Guangqin Zhang; Suhua Qiu; Heming Wei
Journal:  Neurochem Res       Date:  2011-02-22       Impact factor: 3.996

10.  Characterization of single voltage-gated Na+ and Ca2+ channels in apical dendrites of rat CA1 pyramidal neurons.

Authors:  J C Magee; D Johnston
Journal:  J Physiol       Date:  1995-08-15       Impact factor: 5.182

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