Dihydropyridine receptors actively control gating of ryanodine receptors in resting mouse skeletal muscle fibres.

摘要: Key points •  Depolarization of the skeletal muscle membrane elicits a change in configuration dihydropyridine receptors that turn triggers sarcoplasmic reticulum (SR) Ca2+ release through ryanodine receptors. •  At rest, it is assumed, but never demonstrated adult fibres, exert repressive action on keeps them closed state. •  By measuring changes SR voltage-clamp conditions, we report any interventions designed to alter conformation at rest induce an efflux. •  These results show maintain strict control upon resting mouse fibres. Abstract  Contraction triggered by from response depolarization membrane. Depolarization known elicit conformational receptor (DHPR) tubular controls time- and voltage-dependent manner opening (RyR), channel. At assumed RyRs are kept state imposed DHPRs; however, direct RyR gating DHPR has up now been muscle. In this study, monitored slow content using indicator fluo-5N loaded voltage-clamped fibres. We first external removal induced reversible efflux −80 mV prevented refilling following depolarization-evoked depletion. The compound nifedipine similar effects. rate was also shown be controlled within potential range more negative than −50 mV. Finally, intracellular addition produced irreversible highly depleted fact modulated DHPRs Ca2+, voltage demonstrates active