The Ca²⁺ influx through the mammalian skeletal muscle dihydropyridine receptor is irrelevant for muscle performance.

ABSTRACT: Skeletal muscle excitation-contraction (EC) coupling is initiated by sarcolemmal depolarization, which is translated into a conformational change of the dihydropyridine receptor (DHPR), which in turn activates sarcoplasmic reticulum (SR) Ca²⁺ release to trigger muscle contraction. During EC coupling, the mammalian DHPR embraces functional duality, as voltage sensor and L-type Ca²⁺ channel. Although its unique role as voltage sensor for conformational EC coupling is firmly established, the conventional function as Ca²⁺ channel is still enigmatic. Here we show that Ca²⁺ influx via DHPR is not necessary for muscle performance by generating a knock-in mouse where DHPR-mediated Ca²⁺ influx is eliminated. Homozygous knock-in mice display SR

SUBMITTER: Dayal A 

PROVIDER: S-EPMC5589907 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature