Issues

JGP study reveals that adult zebrafish skeletal muscle fibers display the fastest kinetics of excitation–contraction coupling ever measured in vertebrate locomotor muscles.

It is controversial whether the cardiac type-2 ryanodine receptor harboring a catecholaminergic polymorphic ventricular tachycardia-associated point mutation is regulated by luminal or cytosolic Ca²⁺. This commentary discusses new findings supporting the cytosolic Ca²⁺-dependent regulation.

David G. Allen looks at new research from the Nielsen lab.

Melzer discusses a recent JGP study showing that alternative splicing of the skeletal muscle L-type calcium channel impacts on a modulatory effect of its γ subunit.

In skeletal muscle fibers, mitochondria calcium uptake is relevant for metabolic activation, trophic regulation, and apoptosis. It is still debated whether mitochondria can modulate cytosolic calcium transients and contractile performance. Here, we discuss evidence in favor or against this possibility.

This review provides an up-to-date overview of current knowledge on myopathies caused by mutations in proteins participating in excitation–contraction coupling and store-operated Ca²⁺ entry mechanisms in skeletal muscle.

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.

The promiscuity of flecainide underscores its antiarrhythmic efficacy in CPVT: this paper presents a discussion of its mechanisms of action on the cardiac ryanodine receptor (RyR2) and other cardiac excitation–contraction coupling proteins.

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.

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.

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.

The zebrafish displays an escape response powered by superfast contraction of swimming muscle. Idoux et al. show that steps preceding contraction, from action potential firing to increase in intracellular Ca²⁺, display the fastest kinetics ever measured in vertebrate locomotor muscles.

Imaging of glycogen particles in skeletal muscle fibers has revealed a heterogenic subcellular distribution. Nielsen et al. show that spatially distinct pools of glycogen are differentially used by the three main ATPases in skeletal muscle (myosin, SR Ca²⁺, and Na⁺,K⁺ ATPases, respectively).

Postdevelopmental, muscle-specific ablation of Orai1 in mdx mice abolishes excessive constitutive and store-operated Ca²⁺ entry, improves muscular dystrophy pathology, and promotes sarcolemmal integrity, thus demonstrating an important role of enhanced Orai1-mediated Ca²⁺ entry in exacerbating the dystrophic phenotype.

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.

The present numerical modeling study shows that disorder in locations of Ca release units in cardiac pacemaker cells has substantial functional impact by creating release clusters, similar to Poisson clumping, and opportunity of Ca release to propagate within the clusters.

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.

Manno et al. demonstrate a simple, fast, and noninvasive procedure, whereby the lifetimes of autofluorescence excited with visible light and measured by confocal photon counting are used on live skeletal muscle to distinguish type I from type II myofibers.