Premium
SK channels are necessary but not sufficient for denervation‐induced hyperexcitability
Author(s) -
Jacobson David,
Herson Paco S.,
Neelands Torben R.,
Maylie James,
Adelman John P.
Publication year - 2002
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/mus.10280
Subject(s) - denervation , apamin , skeletal muscle , medicine , chemistry , anatomy , endocrinology , neuroscience , potassium channel , biology
Abstract Skeletal muscle hyperexcitability is characteristically associated with denervation. Expression of SK3, a small conductance Ca 2+ ‐activated K + channel (SK channel) in skeletal muscle is induced by denervation, and direct application of apamin, a peptide blocker of SK channels, dramatically reduces hyperexcitability. To investigate the role of SK3 channels in denervation‐ induced hyperexcitability, SK3 expression was manipulated using a transgenic mouse that harbors a tetracycline‐regulated SK3 gene. Electromyographic (EMG) recordings from anterior tibial (AT) muscle showed that denervated muscle from transgenic or wild‐type animals had equivalent hyperexcitability that was blocked by apamin. In contrast, denervated skeletal muscle from SK3tTA mice lacking SK3 channels showed little or no hyperexcitability, similar to results from wild‐type innervated skeletal muscle. However, innervated skeletal muscle from SK3tTA mice containing SK3 channels did not show hyperexcitability. The results demonstrate that SK3 channels are necessary but not sufficient for denervation‐induced skeletal muscle hyperexcitability. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 817–822, 2002