Literature DB >> 8894443

Sodium channel expression: a dynamic process in neurons and non-neuronal cells.

J A Black1, S G Waxman.   

Abstract

Although voltage-gated sodium channels have been most carefully studied in neurons, these channels are also present in nonexcitable cells within the nervous system and outside the nervous system. The mRNAs and protein for rat brain type sodium channels are expressed in both non-neuronal nervous system cells (glial cells) and in some cell types outside the nervous system. In most of these cell types, the expression of sodium channels is dynamic, with the levels and proportions of various sodium channel subtypes changing during development, and in response to injury and upon exposure to neurotrophins. It is likely that, in the near future, we will understand the roles played by sodium channels in each of these cell types, and the regulatory mechanisms that control expression of these channels.

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Year:  1996        PMID: 8894443     DOI: 10.1159/000111403

Source DB:  PubMed          Journal:  Dev Neurosci        ISSN: 0378-5866            Impact factor:   2.984


  16 in total

Review 1.  Regulation of ion channel expression in neural cells by hormones and growth factors.

Authors:  L J Chew; V Gallo
Journal:  Mol Neurobiol       Date:  1998-12       Impact factor: 5.590

2.  Dual tandem promoter elements containing CCAC-like motifs from the tetrodotoxin-resistant voltage-sensitive Na+ channel (rSkM2) gene can independently drive muscle-specific transcription in L6 cells.

Authors:  H Zhang; M N Maldonado; R L Barchi; R G Kallen
Journal:  Gene Expr       Date:  1999

3.  Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons.

Authors:  Raimund I Herzog; Theodore R Cummins; Farshid Ghassemi; Sulayman D Dib-Hajj; Stephen G Waxman
Journal:  J Physiol       Date:  2003-07-03       Impact factor: 5.182

Review 4.  Voltage-gated Na+ channels: multiplicity of expression, plasticity, functional implications and pathophysiological aspects.

Authors:  J K J Diss; S P Fraser; M B A Djamgoz
Journal:  Eur Biophys J       Date:  2004-02-12       Impact factor: 1.733

5.  Slow closed-state inactivation: a novel mechanism underlying ramp currents in cells expressing the hNE/PN1 sodium channel.

Authors:  T R Cummins; J R Howe; S G Waxman
Journal:  J Neurosci       Date:  1998-12-01       Impact factor: 6.167

Review 6.  Sodium channels and pain: from toxins to therapies.

Authors:  Fernanda C Cardoso; Richard J Lewis
Journal:  Br J Pharmacol       Date:  2017-09-02       Impact factor: 8.739

7.  Pharmacological kinetics of BmK AS, a sodium channel site 4-specific modulator on Nav1.3.

Authors:  Zhi-Rui Liu; Jie Tao; Bang-Qian Dong; Gang Ding; Zhi-Jun Cheng; Hui-Qiong He; Yong-Hua Ji
Journal:  Neurosci Bull       Date:  2012-06       Impact factor: 5.203

Review 8.  Transcriptional and posttranslational plasticity and the generation of inflammatory pain.

Authors:  C J Woolf; M Costigan
Journal:  Proc Natl Acad Sci U S A       Date:  1999-07-06       Impact factor: 11.205

9.  Nav1.3 sodium channels: rapid repriming and slow closed-state inactivation display quantitative differences after expression in a mammalian cell line and in spinal sensory neurons.

Authors:  T R Cummins; F Aglieco; M Renganathan; R I Herzog; S D Dib-Hajj; S G Waxman
Journal:  J Neurosci       Date:  2001-08-15       Impact factor: 6.167

Review 10.  Postherpetic neuralgia: from preclinical models to the clinic.

Authors:  Ada Delaney; Lesley A Colvin; Marie T Fallon; Robert G Dalziel; Rory Mitchell; Susan M Fleetwood-Walker
Journal:  Neurotherapeutics       Date:  2009-10       Impact factor: 7.620

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