ArticleThe Journal of physiology1990
Characteristics of Na+ channels and Cl- conductance in resealed muscle fibre segments from patients with myotonic dystrophy.
Article in The Journal of physiology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 89 citations in OpenAlex.
- Afterdischarges in myotonic dystrophy type 1.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- SpecificMolecular therapy. Nucleic acids · 2023Article
- Complications After Dental Sedation: A Myotonic Mystery Case Report.Anesthesia progress · 2022Review
- Myotonic Dystrophy and Anesthetic Challenges: A Case Report and Review.Case reports in anesthesiology · 2019Article
- The golden retriever model of Duchenne muscular dystrophy.Skeletal muscle · 2017Review
- Targeting deregulated AMPK/mTORC1 pathways improves muscle function in myotonic dystrophy type I.The Journal of clinical investigation · 2017Article
- In vivo assessment of muscle membrane properties in myotonic dystrophy.Muscle & nerve · 2016Article
- Epigenetics of the myotonic dystrophy-associated DMPK gene neighborhood.Epigenomics · 2016Article
- Age-dependent chloride channel expression in skeletal muscle fibres of normal and HSA(LR) myotonic mice.The Journal of physiology · 2013Article
- Correction of ClC-1 splicing eliminates chloride channelopathy and myotonia in mouse models of myotonic dystrophy.The Journal of clinical investigation · 2007Article
- Inhibition of anion channels derived from mitochondrial membranes of the rat heart by stilbene disulfonate--DIDS.Journal of bioenergetics and biomembranes · 2007Article
- Gene expression analysis in myotonic dystrophy: indications for a common molecular pathogenic pathway in DM1 and DM2.Gene expression · 2007Article
- Sodium channel isoform-specific effects of halothane: protein kinase C co-expression and slow inactivation gating.British journal of pharmacology · 2000Article
- Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.The Journal of clinical investigation · 1997Article
- Neural control of the expression of a Ca(2+)-activated K+ channel involved in the induction of myotonic-like characteristics.Cellular and molecular neurobiology · 1996Article
- Modulation of skeletal muscle sodium channels by human myotonin protein kinase.The Journal of clinical investigation · 1995Article
- Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.Biophysical journal · 1993Article
- Deficiency of Na+/K(+)-ATPase and sarcoplasmic reticulum Ca(2+)-ATPase in skeletal muscle and cultured muscle cells of myotonic dystrophy patients.The Biochemical journal · 1993Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Electrical and contractile properties of resealed fibre segments were investigated by a variety of in vitro techniques. The preparations were removed from skeletal muscles of normal subjects and of eight patients with myotonic dystrophy. 2. Several hours after removal, fibre segments from normal subjects and those patients in whom myotonia was the primary symptom had resting membrane potentials of approximately -80 mV. In contrast, fibre segments obtained from patients in whom muscle dystrophy was more expressed were depolarized (-60 to -70 mV). 3. Contractions induced in fibre segments of myotonic muscle which had normal potentials were characterized by slowed relaxation which was due to electrical after-activity. 4. After single stimuli, long-lasting (3-100) runs of action potentials were recorded intracellularly from the myotonic muscle. In some of these fibre segments complex repetitive discharges were observed: multiple sites of locally gated currents were identified. 5. The three-electrode voltage clamp was used to determine the total membrane conductance, gm, and the ion component conductances. All fibres of a particular patient had similar conductances. However, the Cl- conductance varied from patient to patient from normal (74% of gm) to low values (30% of gm). The K+ conductance was normal in all fibres of all patients. 6. The patch-clamp technique was used to record currents through single Na+ channels of the sarcolemma. After treatment of the fibre segments with collagenase gigaohm seals were routinely obtained. The rate of success was greater when using the cell-attached mode than the inside-out mode. 7. Sodium channel currents were elicited by depolarizing voltage steps which produced an initial burst of Na+ channel openings. Up to ten channels were activated simultaneously when the patch was depolarized to potentials more positive than -30 mV. The Na+ channels re-opened very rarely in controls. The macroscopic sodium current, INa, was reconstructed by averaging depolarizing pulses. The time constant of rapid decay of INa reflecting macroscopic inactivation, the onset of INa and the amplitude of INa were voltage dependent. The mean amplitude of the current produced by re-openings was on average only 0.11 +/- 0.04% of the amplitude of the peak current. 8. Late openings of the Na+ channels were frequent in patches on the myotonic fibre segments. The amplitude of the current produced by re-openings was as high as about 0.75 +/- 0.11% of the amplitude of the peak current.(ABSTRACT TRUNCATED AT 400 WORDS)
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