ArticleThe Journal of physiology2008
Expression of small-conductance calcium-activated potassium channels (SK3) in skeletal muscle: regulation by muscle activity.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Changes in motor unit conduction velocity after unilateral lower-limb suspension and active recovery are correlated with muscle ion channel gene expression.Experimental physiology · 2025Article
- Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Myotonic Dystrophy Type 1 Management and Therapeutics.Current treatment options in neurology · 2016Review
- Emerging role of the calcium-activated, small conductance, SK3 K+ channel in distal tubule function: regulation by TRPV4.PloS one · 2014Article
- Chronic muscle stimulation improves muscle function and reverts the abnormal surface EMG pattern in myotonic dystrophy: a pilot study.Journal of neuroengineering and rehabilitation · 2013Article
- Analysis of Single Nucleotide Polymorphisms (SNPs) of the small-conductance calcium activated potassium channel (SK3) gene as genetic modifier of the cardiac phenotype in myotonic dystrophy type 1 patients.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2008Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type 3 small conductance calcium-activated potassium channel (SK3) is expressed in embryonic and adult denervated skeletal muscles where it contributes to hyperexcitability. This study aimed at determining the role of muscle activity in regulating SK3 channels. Soleus muscles of adult rats were denervated by cutting the sciatic nerve. In reinnervation studies, the soleus nerve was crushed: in one group, muscles were reinnervated with electrically silent axons, by chronic sciatic nerve perfusion with tetrodotoxin. Several groups of denervated muscles were subjected to chronic direct electrical stimulation, using either fast (100 Hz) or slower patterns (20 or 30 Hz). The SK3 mRNA and protein levels in soleus muscle were determined by reverse transcriptional-PCR, Western blot and immunofluorescence. Both denervated and reinnervated-paralysed soleus muscles displayed similar up-regulation of SK3 mRNA and protein. Reinnervation with electrically active axons instead inhibited SK3 up-regulation. Chronic muscle direct stimulation in vivo, irrespective of the pattern used, reversed the denervation-induced up-regulation of SK3 expression or prevented it when initiated at the time of denervation. Chronic electrical stimulation of denervated muscles also completely prevented the development of the after-hyperpolarization (AHP) following the action potential, normally induced in the muscle fibres by denervation. We conclude that action potential activity evoked by motor neurones in muscle fibres is both necessary and sufficient to account for the physiological down-regulation of SK3 channels in the non-junctional membrane of skeletal muscle.
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