Di-4-ANEPPS Modulates Electrical Activity and Progress of Myocardial Ischemia in Rabbit Isolated Heart.

Aims: Although voltage-sensitive dye di-4-ANEPPS is a common tool for mapping cardiac electrical activity, reported effects on electrophysiological parameters are rather. The main goals of the study were to reveal effects of the dye on rabbit isolated heart and to verify, whether rabbit isolated heart stained with di-4-ANEPPS is a suitable tool for myocardial ischemia investigation.

Methods And Results: Study involved experiments on stained ( = 9) and non-stained ( = 11) Langendorff perfused rabbit isolated hearts.

Role of glucocorticoid- and monoamine-metabolizing enzymes in stress-related psychopathological processes.

Glucocorticoid signaling is fundamental in healthy stress coping and in the pathophysiology of stress-related diseases, such as post-traumatic stress disorder (PTSD). Glucocorticoids are metabolized by cytochrome P450 (CYP) as well as 11-β-hydroxysteroid dehydrogenase type 1 (11βHSD1) and 2 (11βHSD2). Acute stress-induced increase in glucocorticoid concentrations stimulates the expression of several CYP sub-types.

Correction to: Four novel interaction partners demonstrate diverse modulatory effects on voltage-gated Ca2.2 Ca channels.

The article was originally published with one author missing. The name of the co-author Roman Moravcik was inadvertently omitted. His name and affiliation have now been added to the author list.

Four novel interaction partners demonstrate diverse modulatory effects on voltage-gated Ca2.2 Ca channels.

Voltage-gated Ca channels are embedded in a network of protein interactions that are fundamental for channel function and modulation. Different strategies such as high-resolution quantitative MS analyses and yeast-two hybrid screens have been used to uncover these Ca channel nanodomains. We applied the yeast split-ubiquitin system with its specific advantages to search for interaction partners of the Ca2.

Cellular and molecular mechanisms underlying the treatment of depression: focusing on hippocampal G-protein-coupled receptors and voltage-dependent calcium channels.

Depression is a brain disorder characterized by severe emotional, cognitive, neuroendocrine and somatic dysfunction. Although the latest generation of antidepressant drugs has improved clinical efficacy and safety, the onset of their clinical effect is significantly delayed after treatment commencement, and a large number of patients exhibit inadequate response to these drugs and/or depression relapse even following initially successful treatment. It is therefore essential to develop new antidepressant drugs and/or adjuncts to existing ones.

Effects of AP39, a novel triphenylphosphonium derivatised anethole dithiolethione hydrogen sulfide donor, on rat haemodynamic parameters and chloride and calcium Cav3 and RyR2 channels.

H2S donor molecules have the potential to be viable therapeutic agents. The aim of this current study was (i) to investigate the effects of a novel triphenylphosphonium derivatised dithiolethione (AP39), in the presence and absence of reduced nitric oxide bioavailability and (ii) to determine the effects of AP39 on myocardial membrane channels; CaV3, RyR2 and Cl(-). Normotensive, L-NAME- or phenylephrine-treated rats were administered Na2S, AP39 or control compounds (AP219 and ADT-OH) (0.

TGFβ1 downregulates neurite outgrowth, expression of Ca2+ transporters, and mitochondrial dynamics of in vitro cerebellar granule cells.

Acute injury to central nervous system (CNS) triggers neurodegenerative processes that can result in serious damage or complete loss of function. After injury, production of transforming growth factor β1 (TGFβ1) increases and initiates creation of a fibrotic scar that prevents normal growth, plasticity, and recovery of damaged neurons. Administration of TGFβ1 antagonists can prevent its pathological effects.

Bisphenol A differently inhibits CaV3.1, Ca V3.2 and Ca V3.3 calcium channels.

Bisphenol A (BPA) is a widespread environmental contaminant detected in urine of 93 % of investigated US population. Recent epidemiological studies found correlation between BPA exposure and diseases including cardiovascular and neuronal disorders. BPA targets include hormone receptors and voltage-dependent ion channels.

Calcium transporters and their role in the development of neuronal disease and neuronal damage.

Neurodegeneration comprises assembly of pathophysiological events that gives rise to a progressive loss of neuronal structure and function including cellular damage, diseases development or cellular death. Neurons respond by adjusting signaling pathways, from gene expression to morphological changes. In most of these processes, Ca2+ signaling plays a pivotal role.

The effect of the outermost basic residues in the S4 segments of the Ca(V)3.1 T-type calcium channel on channel gating.

The contribution of voltage-sensing S4 segments in domains I to IV of the T-type Ca(V)3.1 calcium channel to channel gating was investigated by the replacement of the uppermost charged arginine residues by neutral cysteines. In each construct, either a single (R180C, R834C, R1379C or R1717C) or a double (two adjacent domains) mutation was introduced.

Ultrastructural remodeling of fast skeletal muscle fibers induced by invalidation of creatine kinase.

Understanding muscle adaptation to various stimuli is difficult because of the complex nature of stimuli and responses. In particular, responses to perturbations in energy metabolism require careful examination, because they may involve both structural and functional elements. To estimate the structural component of the myocyte adaptation to energetic deficiency, we used transgenic mice with blocked expression of mitochondrial and cytosolic creatine kinases (CK).

Joint participation of mitochondria and sarcoplasmic reticulum in the formation of tubular aggregates in gastrocnemius muscle of CK-/- mice.

Tubular aggregates are specific subcellular structures that appear in skeletal muscle fibres under different pathological conditions. The origin of the tubular aggregates is generally ascribed to proliferating membranes of sarcoplasmic reticulum. There are, however, histochemical indications for the presence of mitochondrial enzymes in tubular aggregates suggesting contribution of mitochondria to the genesis of tubular aggregates.