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How and why are calcium currents curtailed in the skeletal muscle voltage‐gated calcium channels?
Author(s) -
Flucher Bernhard E.,
Tuluc Petronel
Publication year - 2017
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp273423
Subject(s) - skeletal muscle , gating , t type calcium channel , calcium , n type calcium channel , voltage dependent calcium channel , calcium channel , muscle contraction , biophysics , chemistry , microbiology and biotechnology , r type calcium channel , voltage gated ion channel , calcium signaling , ion channel , membrane potential , calcium in biology , contraction (grammar) , intracellular , biology , biochemistry , anatomy , endocrinology , receptor , organic chemistry
Voltage‐gated calcium channels represent the sole mechanism converting electrical signals of excitable cells into cellular functions such as contraction, secretion and gene regulation. Specific voltage‐sensing domains detect changes in membrane potential and control channel gating. Calcium ions entering through the channel function as second messengers regulating cell functions, with the exception of skeletal muscle, where Ca V 1.1 essentially does not function as a channel but activates calcium release from intracellular stores. It has long been known that calcium currents are dispensable for skeletal muscle contraction. However, the questions as to how and why the channel function of Ca V 1.1 is curtailed remained obscure until the recent discovery of a developmental Ca V 1.1 splice variant with normal channel functions. This discovery provided new means to study the molecular mechanisms regulating the channel gating and led to the understanding that in skeletal muscle, calcium currents need to be restricted to allow proper regulation of fibre type specification and to prevent mitochondrial damage.