ArticleThe Journal of physiology2002
Effects of chloride transport on bistable behaviour of the membrane potential in mouse skeletal muscle.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Targeted Therapies for Skeletal Muscle Ion Channelopathies: Systematic Review and Steps Towards Precision Medicine.Journal of neuromuscular diseases · 2021Pooled it
- Mechanisms underlying the distinct K+ dependencies of periodic paralysis.The Journal of general physiology · 2025Article
- Periodic paralysis.Handbook of clinical neurology · 2024Review
- Bistability of somatic pattern memories: stochastic outcomes in bioelectric circuits underlying regeneration.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021Review
- Gene regulatory networks exhibit several kinds of memory: quantification of memory in biological and random transcriptional networks.iScience · 2021Article
- Myotonia in a patient with a mutation in an S4 arginine residue associated with hypokalaemic periodic paralysis and a concomitant synonymous CLCN1 mutation.Scientific reports · 2019Article
- Recovery from acidosis is a robust trigger for loss of force in murine hypokalemic periodic paralysis.The Journal of general physiology · 2019Article
- Elevation of extracellular osmolarity improves signs of myotonia congenita in vitro: a preclinical animal study.The Journal of physiology · 2019Article
- Kir2.1 channels set two levels of resting membrane potential with inward rectification.Pflugers Archiv : European journal of physiology · 2018Article
- Sodium Channelopathies of Skeletal Muscle.Handbook of experimental pharmacology · 2018Review
- Kir2.1 and K2P1 channels reconstitute two levels of resting membrane potential in cardiomyocytes.The Journal of physiology · 2017Article
- Role of physiological ClC-1 Cl- ion channel regulation for the excitability and function of working skeletal muscle.The Journal of general physiology · 2016Review
- Genetic neurological channelopathies: molecular genetics and clinical phenotypes.Journal of neurology, neurosurgery, and psychiatry · 2016Review
- Ionic imbalance, in addition to molecular crowding, abates cytoskeletal dynamics and vesicle motility during hypertonic stress.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Altered and dynamic ion selectivity of K+ channels in cell development and excitability.Trends in pharmacological sciences · 2014Review
- Beneficial effects of bumetanide in a CaV1.1-R528H mouse model of hypokalaemic periodic paralysis.Brain : a journal of neurology · 2013Article
- Bumetanide prevents transient decreases in muscle force in murine hypokalemic periodic paralysis.Neurology · 2013Article
- Inward flux of lactate⁻ through monocarboxylate transporters contributes to regulatory volume increase in mouse muscle fibres.PloS one · 2013Article
- Novel insights into the pathomechanisms of skeletal muscle channelopathies.Current neurology and neuroscience reports · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lumbrical skeletal muscle fibres of mice exhibited electrically bistable behaviour due to the nonlinear properties of the inwardly rectifying potassium conductance. When the membrane potential (V(m)) was measured continuously using intracellular microelectrodes, either a depolarization or a hyperpolarization was observed following reduction of the extracellular potassium concentration (K+o) from 5.7 mM to values in the range 0.76-3.8 mM, and V(m) showed hysteresis when K+o was slowly decreased and then increased within this range. Hypertonicity caused membrane depolarization by enhancing chloride import through the Na+-K+-2Cl- cotransporter and altered the bistable behaviour of the muscle fibres. Addition of bumetanide, a potent inhibitor of the Na+-K+-2Cl- cotransporter, and of anthracene-9-carboxylic acid, a blocker of chloride channels, caused membrane hyperpolarization particularly under hypertonic conditions, and also altered the bistable behaviour of the cells. Hysteresis loops shifted with hypertonicity to higher K+o values and with bumetanide to lower values. The addition of 80 microM BaCl2 or temperature reduction from 35 to 27 degrees C induced a depolarization of cells that were originally hyperpolarized. In the K+o range of 5.7-22.8 mM, cells in isotonic media (289 mmol x kg(-1)) responded nearly Nernstianly to K+o reduction, i.e. 50 mV per decade; in hypertonic media this dependence was reduced to 36 mV per decade (319 mmol x kg(-1)) or to 31 mV per decade (340 mmol x kg(-1)). Our data can explain apparent discrepancies in DeltaV(m) found in the literature. We conclude that chloride import through the Na+-K+-2Cl- cotransporter and export through Cl- channels influenced the V(m) and the bistable behaviour of mammalian skeletal muscle cells. The possible implication of this bistable behaviour in hypokalaemic periodic paralysis is discussed.
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