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Fibrillation potentials of denervated rat skeletal muscle are associated with expression of cardiac-type voltage-gated sodium channel isoform Nav1.5.

Authors: Sekiguchi, K  Kanda, F  Mitsui, S  Kohara, N  Chihara, K 
Citation: Sekiguchi K, etal., Clin Neurophysiol. 2012 Feb 13.
Pubmed: (View Article at PubMed) PMID:22336133
DOI: Full-text: DOI:10.1016/j.clinph.2012.01.002

OBJECTIVE: The molecular mechanisms underlying fibrillation potentials are still unclear. We hypothesised that expression of the cardiac-type voltage-gated sodium channel isoform Nav1.5 in denervated rat skeletal muscle is associated with the generation of such potentials. METHODS: Muscle samples were extracted and analysed biologically from surgically denervated rat extensor digitorum longus muscle after concentric needle electromyographic recording at various time points after denervation (4h to 6days). RESULTS: Both nav1.5 messenger RNA (mRNA) signal on northern blotting and Nav1.5 protein expression on immunohistochemistry appeared on the second day after denervation, exactly when fibrillation potentials appeared. Administration of lidocaine, which has much stronger affinity for sodium channels in cardiac muscle than for those in skeletal muscle, dramatically decreased fibrillation potentials, but had no effect on contralateral compound muscle action potentials. CONCLUSIONS: Expression of Nav1.5 participates in the generation of fibrillation potentials in denervated rat skeletal muscle. SIGNIFICANCE: We proposed an altered expression of voltage-gated sodium channel isoforms as a novel mechanism to explain the occurrence of fibrillation potentials following skeletal muscle denervation.

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RGD Object Information
RGD ID: 6484222
Created: 2012-06-14
Species: All species
Last Modified: 2012-06-14
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.