ArticleThe Journal of physiology2011
Gating behaviour of sodium currents in adult mouse muscle recorded with an improved two-electrode voltage clamp.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Dissecting Gap Junctional and Ephaptic Contributions to Electrical Conduction in a Novel Cardiomyocyte Pair Model.bioRxiv : the preprint server for biology · 2026Article
- Voltage Gated Ion Channels and Sleep.The Journal of membrane biology · 2024Review
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- New Challenges Resulting From the Loss of Function of NaFrontiers in pharmacology · 2021Review
- A four-electrode method to study dynamics of ion activity and transport in skeletal muscle fibers.The Journal of general physiology · 2019Article
- Rapsyn facilitates recovery from desensitization in fetal and adult acetylcholine receptors expressed in a muscle cell line.The Journal of physiology · 2019Article
- Sodium Channelopathies of Skeletal Muscle.Handbook of experimental pharmacology · 2018Review
- Acute Elevated Glucose Promotes Abnormal Action Potential-Induced CaJournal of diabetes research · 2017Article
- Mice with an NaV1.4 sodium channel null allele have latent myasthenia, without susceptibility to periodic paralysis.Brain : a journal of neurology · 2016Article
- Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Skeletal muscle · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Resurgent current of voltage-gated Na(+) channels.The Journal of physiology · 2014Review
- Disrupted coupling of gating charge displacement to Na+ current activation for DIIS4 mutations in hypokalemic periodic paralysis.The Journal of general physiology · 2014Article
- Combined modifications of mexiletine pharmacophores for new lead blockers of Na(v)1.4 channels.Biophysical journal · 2013Article
- A calcium channel mutant mouse model of hypokalemic periodic paralysis.The Journal of clinical investigation · 2012Article
- The delayed rectifier potassium conductance in the sarcolemma and the transverse tubular system membranes of mammalian skeletal muscle fibers.The Journal of general physiology · 2012Article
- Voltage clamp methods for the study of membrane currents and SR Ca(2+) release in adult skeletal muscle fibres.Progress in biophysics and molecular biology · 2012Review
- Left-shifted nav channels in injured bilayer: primary targets for neuroprotective nav antagonists?Frontiers in pharmacology · 2012Article
- A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis.The Journal of clinical investigation · 2011Article
- The Na conductance in the sarcolemma and the transverse tubular system membranes of mammalian skeletal muscle fibers.The Journal of general physiology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Muscle contraction is triggered by the spread of an action potential along the fibre. The ionic current to generate the action potential is conducted through voltage-activated sodium channels, and mutations of these channels are known to cause several human muscle disorders. Mouse models have been created by introducing point mutations into the sodium channel gene. This achievement has created the need for a high-fidelity technique to record sodium currents from intact mouse muscle fibres. We have optimized a two-electrode voltage clamp, using sharp microelectrodes to preserve the myoplasmic contents. The voltage-dependent behaviour of sodium channel activation, inactivation and slow-inactivation were characterized. The voltage range for these gating behaviours was remarkably hyperpolarized, in comparison to studies in artificial expression systems. These results provide normative data for sodium channels natively expressed in mouse muscle and illustrate the need to modify model simulations of muscle excitability to account for the hyperpolarized shift.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.