Dysregulation of mitochondrial calcium signaling and superoxide flashes cause mitochondrial genomic DNA damage in Huntington disease.

Huntington disease (HD) is an inherited, fatal neurodegenerative disorder characterized by the progressive loss of striatal medium spiny neurons. Indications of oxidative stress are apparent in brain tissues from both HD patients and HD mouse models; however, the origin of this oxidant stress remains a mystery. Here, we used a yeast artificial chromosome transgenic mouse model of HD (YAC128) to investigate the potential connections between dysregulation of cytosolic Ca(2+) signaling and mitochondrial oxidative damage in HD cells.

[Effects of 50 Hz sinusoidal magnetic field on Ca2+ release channel ryanodine receptor of sarcoplasmic reticulum vesicles].

Objective: To investigate the effects of sinusoidal magnetic field on isolated sarcoplasmic reticulum (SR) calcium release channel (RyR1) function.

Methods: With the Ca2+ dynamic spectrum and isotope labeled methods, the Ca2+ release and [(3)H]-Ryanodine binding, the initial rates of NADH oxidation and the production of superoxide of SR exposed to 50 Hz sinusoidal magnetic field (MF) were investigated respectively.

Results: 0.

Swim training sensitizes myocardial response to insulin: role of Akt-dependent eNOS activation.

Objectives: Physical activity has been well known to benefit heart function. The improved autonomic nervous activity is considered to be mainly responsible for this beneficial effect. However, the precise mechanism behind the intrinsic myocardial responsiveness to exercise is still unclear.

Ca2+ sparks and Ca2+ glows in superior cervical ganglion neurons.

Aim: Ca2+ release from the endoplasmic reticulum (ER) is an integral component of neuronal Ca2+ signaling. The present study is to investigate properties of local Ca2+ release events in superior cervical ganglion (SCG) neurons.

Methods: Primary cultured SCG neurons were prepared from neonatal rats (P3-P7).

Cross-talk between calcium and reactive oxygen species signaling.

Calcium [Ca2+] and reactive oxygen species (ROS) constitute the most important intracellular signaling molecules participating in the regulation and integration of diverse cellular functions. Here we briefly review cross-talk between the two prominent signaling systems that finely tune the homeostasis and integrate functionality of Ca2+ and ROS in different types of cells. Ca2+ modulates ROS homeostasis by regulating ROS generation and annihilation mechanisms in both the mitochondria and the cytosol.

Calcium signaling in physiology and pathophysiology.

Calcium ions are the most ubiquitous and pluripotent cellular signaling molecules that control a wide variety of cellular processes. The calcium signaling system is represented by a relatively limited number of highly conserved transporters and channels, which execute Ca2+ movements across biological membranes and by many thousands of Ca2+-sensitive effectors. Molecular cascades, responsible for the generation of calcium signals, are tightly controlled by Ca2+ ions themselves and by genetic factors, which tune the expression of different Ca2+-handling molecules according to adaptational requirements.

The timing of endocytosis after activation of a G-protein-coupled receptor in a sensory neuron.

Endocytosis is a fundamental cellular event in membrane retrieval after exocytosis and in the regulation of receptor-mediated signal transduction. In contrast to the well-studied depolarization-induced membrane recycling, little is known about the kinetics of ligand-induced endocytosis of G-protein-coupled receptors in neurons. Here we investigated the kinetics of ligand-receptor binding-induced endocytosis in rat sensory neurons using a membrane capacitance assay.

[Microscopic mechanism of excitation-contraction coupling in cardiac myocytes].

Cardiac excitation-contraction coupling (ECC) is, in essence, a communication process between sarcolemmal voltage-dependent L-type calcium channels (LCCs) and ryanodine receptors (RyRs) of sarcoplasmic reticulum (SR) by the mechanism of calcium-induced calcium release (CICR). Recent advances displayed more information about the microscopic signaling between LCCs and RyRs. In calcium release couplons, the calcium influx through the opening of LCCs by membrane depolarization forms calcium sparklets locally which then act on the adjacent SR RyRs.

Blockade of paeoniflorin on sodium current in mouse hippocampal CA1 neurons.

Aim: To study the blockade of paeoniflorin (Pae) on I(Na) in the acutely isolated hippocampus neurons of mice.

Methods: The whole-cell patch clamp technique was used.

Results: Pae inhibited I(Na) in frequency-dependent and concentration-dependent manners, with an IC50 of 271 micromol/L.