Issues

Guarina et al. discuss recent findings suggesting that the high reproducibility of cardiac contraction emerges from high Ca²⁺ signaling variability at multiple levels due to stochastic fluctuations in multiple processes in time and space, but manifests as reliable Ca²⁺ transients during EC coupling.

CPVT-linked RYR2 mutations are prone to induce spontaneous Ca²⁺ release from the ER, which is associated with arrhythmias. Kurebayashi et al. used experiments and simulations to explore the mechanisms relating cytosolic Ca²⁺-dependent activity by RYR2 mutations and spontaneous Ca²⁺ release.

Xue et al. show that alteration of the Ca²⁺ clock by a mechanism involving CaMKII hypoactivation contributes to depression of the intrinsic pacemaker function of the sinoatrial node (SAN) in a mouse model of heart failure.

Barclay and Launikonis developed a mathematical model to quantify the cycling of Ca²⁺ within muscle cells and the heat produced by that process. That heat contributes to the resting heat production of muscles and thus to the maintenance of body temperature.

Muscle junctophilins 1 and 2 and neuronal junctophilins 3 and 4 differ in sequence and in interactions with RYR1. Junctophilin 2 has been shown to support voltage-induced calcium release. Perni and Beam show that junctophilins 1 and 3 also support such a release, but that junctophilin 4 does not.

El Ghaleb et al. analyzed the effects of the γ₁ subunit on current properties and expression of the adult (Ca_V1.1a) and embryonic (Ca_V1.1e) calcium channel splice variants, demonstrating that γ₁ reduces the current amplitude in a splicing-dependent manner.

This communication investigates the effect of extracellular BTP2 on electrically evoked Ca²⁺ release in intact skeletal muscle fibers. The results demonstrate that acute exposure to 10 μM BTP2 does not significantly affect the magnitude or kinetics of electrically evoked Ca²⁺ release.