Skeletal muscle and small-conductance calcium-activated potassium channels

David Pribnow, Teresa Johnson-Pais, Chris T. Bond, John Keen, Robert A. Johnson, Aaron Janowsky, Christopher Silvia, Mathew Thayer, James Maylie, John P. Adelman

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

Skeletal muscle becomes hyperexcitable following denervation and when cultured in the absence of nerve cells. In these circumstances, the bee venom peptide toxin apamin, a blocker of small-conductance calcium-activated potassium (SK) channels, dramatically reduces the hyperexcitability. In this report, we show that SK3 channels are expressed in denervated skeletal muscle and in L6 cells. Action potentials evoked from normal innervated rat skeletal muscle did not exhibit an afterhyperpolarization, indicating a lack of SK channel activity; very low levels of apamin binding sites, SK3 protein, or SK3 mRNA were present. However, denervation resulted in apamin-sensitive afterhyperpolarizations and increased apamin binding sites, SK3 protein, and SK3 mRNA. Cultured rat L6 myoblasts and differentiated L6 myotubes contained similar levels of SK3 mRNA, although apamin-sensitive SK currents and apamin binding sites were detected only following myotube differentiation. Therefore, different molecular mechanisms govern SK3 expression levels in denervated muscle compared with muscle cells differentiated in culture.

Original languageEnglish (US)
Pages (from-to)742-750
Number of pages9
JournalMuscle and Nerve
Volume22
Issue number6
DOIs
StatePublished - Jun 1 1999

Keywords

  • Apamin
  • Denervation
  • Hyperexcitability
  • Myotubes
  • SK channels

ASJC Scopus subject areas

  • Physiology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Physiology (medical)

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