Literature DB >> 20038809

Sodium channels gone wild: resurgent current from neuronal and muscle channelopathies.

Stephen C Cannon1, Bruce P Bean.   

Abstract

Voltage-dependent sodium channels are the central players in the excitability of neurons, cardiac muscle, and skeletal muscle. Hundreds of mutations in sodium channels have been associated with human disease, particularly genetic forms of epilepsy, arrhythmias, myotonia, and periodic paralysis. In this issue of the JCI, Jarecki and colleagues present evidence suggesting that many such mutations alter the gating of sodium channels to produce resurgent sodium current, an unusual form of gating in which sodium channels reopen following an action potential, thus promoting the firing of another action potential (see the related article beginning on page 369). The results of this study suggest a widespread pathophysiological role for this mechanism, previously described to occur normally in only a few types of neurons.

Entities:  

Mesh:

Substances:

Year:  2009        PMID: 20038809      PMCID: PMC2798702          DOI: 10.1172/JCI41340

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  20 in total

1.  Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms.

Authors:  I M Raman; B P Bean
Journal:  Biophys J       Date:  2001-02       Impact factor: 4.033

2.  A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.

Authors:  J W West; D E Patton; T Scheuer; Y Wang; A L Goldin; W A Catterall
Journal:  Proc Natl Acad Sci U S A       Date:  1992-11-15       Impact factor: 11.205

3.  Resurgent Na currents in four classes of neurons of the cerebellum.

Authors:  Fatemeh S Afshari; Krzysztof Ptak; Zayd M Khaliq; Tina M Grieco; N Traverse Slater; Donald R McCrimmon; Indira M Raman
Journal:  J Neurophysiol       Date:  2004-06-22       Impact factor: 2.714

Review 4.  Voltage-gated ion channels and hereditary disease.

Authors:  F Lehmann-Horn; K Jurkat-Rott
Journal:  Physiol Rev       Date:  1999-10       Impact factor: 37.312

5.  On the repetitive discharge in myotonic muscle fibres.

Authors:  R H Adrian; S H Bryant
Journal:  J Physiol       Date:  1974-07       Impact factor: 5.182

6.  Na+ channels must deactivate to recover from inactivation.

Authors:  C C Kuo; B P Bean
Journal:  Neuron       Date:  1994-04       Impact factor: 17.173

7.  Resurgent sodium current and action potential formation in dissociated cerebellar Purkinje neurons.

Authors:  I M Raman; B P Bean
Journal:  J Neurosci       Date:  1997-06-15       Impact factor: 6.167

8.  A role for phosphorylation in the maintenance of resurgent sodium current in cerebellar purkinje neurons.

Authors:  Tina M Grieco; Fatemeh S Afshari; Indira M Raman
Journal:  J Neurosci       Date:  2002-04-15       Impact factor: 6.167

9.  Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice.

Authors:  Michael Tri H Do; Bruce P Bean
Journal:  J Neurophysiol       Date:  2004-03-31       Impact factor: 2.714

10.  Two cases of adynamia episodica hereditaria: in vitro investigation of muscle cell membrane and contraction parameters.

Authors:  F Lehmann-Horn; R Rüdel; K Ricker; H Lorković; R Dengler; H C Hopf
Journal:  Muscle Nerve       Date:  1983-02       Impact factor: 3.217

View more
  13 in total

1.  Fast-onset long-term open-state block of sodium channels by A-type FHFs mediates classical spike accommodation in hippocampal pyramidal neurons.

Authors:  Kumar Venkatesan; Yue Liu; Mitchell Goldfarb
Journal:  J Neurosci       Date:  2014-11-26       Impact factor: 6.167

2.  Increased Resurgent Sodium Currents in Nav1.8 Contribute to Nociceptive Sensory Neuron Hyperexcitability Associated with Peripheral Neuropathies.

Authors:  Yucheng Xiao; Cindy Barbosa; Zifan Pei; Wenrui Xie; Judith A Strong; Jun-Ming Zhang; Theodore R Cummins
Journal:  J Neurosci       Date:  2019-01-07       Impact factor: 6.167

Review 3.  Channelopathies from mutations in the cardiac sodium channel protein complex.

Authors:  Graham S Adsit; Ravi Vaidyanathan; Carla M Galler; John W Kyle; Jonathan C Makielski
Journal:  J Mol Cell Cardiol       Date:  2013-04-01       Impact factor: 5.000

Review 4.  Novel insights into the pathomechanisms of skeletal muscle channelopathies.

Authors:  James A Burge; Michael G Hanna
Journal:  Curr Neurol Neurosci Rep       Date:  2012-02       Impact factor: 5.081

Review 5.  Pain as a channelopathy.

Authors:  Ramin Raouf; Kathryn Quick; John N Wood
Journal:  J Clin Invest       Date:  2010-11-01       Impact factor: 14.808

Review 6.  Murine Electrophysiological Models of Cardiac Arrhythmogenesis.

Authors:  Christopher L-H Huang
Journal:  Physiol Rev       Date:  2017-01       Impact factor: 37.312

Review 7.  Neurological perspectives on voltage-gated sodium channels.

Authors:  Niels Eijkelkamp; John E Linley; Mark D Baker; Michael S Minett; Roman Cregg; Robert Werdehausen; François Rugiero; John N Wood
Journal:  Brain       Date:  2012-09       Impact factor: 13.501

8.  Cold aggravates abnormal excitability of motor axons in oxaliplatin-treated patients.

Authors:  Kristine Bennedsgaard; Lise Ventzel; Peter Grafe; Jenny Tigerholm; Andreas C Themistocleous; David L Bennett; Hatice Tankisi; Nanna B Finnerup
Journal:  Muscle Nerve       Date:  2020-03-20       Impact factor: 3.217

9.  Selective Targeting of Nav1.7 with Engineered Spider Venom-Based Peptides.

Authors:  Robert A Neff; Alan D Wickenden
Journal:  Channels (Austin)       Date:  2021-12       Impact factor: 2.581

10.  Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons.

Authors:  Cindy Barbosa; Zhi-Yong Tan; Ruizhong Wang; Wenrui Xie; Judith A Strong; Reesha R Patel; Michael R Vasko; Jun-Ming Zhang; Theodore R Cummins
Journal:  Mol Pain       Date:  2015-09-25       Impact factor: 3.395

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.