The mammalian skeletal muscle DHPR has larger Ca²⁺ conductance and is phylogenetically ancient to the early ray-finned fish sterlet (Acipenser ruthenus).

ABSTRACT: The L-type Ca²⁺ channel or dihydropyridine receptor (DHPR) in vertebrate skeletal muscle is responsible for sensing sarcolemmal depolarizations and transducing this signal to the sarcoplasmic Ca²⁺ release channel RyR1 via conformational coupling to initiate muscle contraction. During this excitation-contraction (EC) coupling process there is a slow Ca²⁺ current through the mammalian DHPR which is fully missing in euteleost fishes. In contrast to ancestral evolutionary stages where skeletal muscle EC coupling is still depended on Ca²⁺-induced Ca²⁺-release (CICR), it is possible that the DHPR Ca²⁺ conductivity during mammalian (conformational) EC coupling was retained as an evolutionary remnant (vestigiality). Here, we wanted

SUBMITTER: Schrotter K 

PROVIDER: S-EPMC5538450 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature