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Skeletal muscle and small‐conductance calcium‐activated potassium channels
Author(s) -
Pribnow David,
JohnsonPais Teresa,
Bond Chris T.,
Keen John,
Johnson Robert A.,
Janowsky Aaron,
Silvia Christopher,
Thayer Mathew,
Maylie James,
Adelman John P.
Publication year - 1999
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199906)22:6<742::aid-mus11>3.0.co;2-1
Subject(s) - calcium activated potassium channel , skeletal muscle , potassium , calcium , conductance , potassium channel , chemistry , biophysics , medicine , anatomy , biology , physics , organic chemistry , condensed matter physics
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. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 742–750, 1999.