The proper intracellular Ca(2+) signaling is essential for normal cell functions and organ development, and the maintaining Ca(2+) homeostasis in cardiac myocytes is of functional importance for the intact heart. As the first functional organ in the vertebrate embryo, the heart is continuously remodeled and maintains its physiologic pumping function in response to increasing circulatory demands. The expressions of Ca(2+) handing proteins in the embryonic heart, however, are different from those in neonatal and adult hearts, which means that the regulation of Ca(2+) transients in embryonic cardiomyocytes is different from that in adult cardiac myocytes. Recent advances in molecular and cellular biology, as well as the application of embryonic stem cell differentiation system, have made progress in uncovering the regulation of Ca(2+) homeostasis during cardiomyogenesis. This paper briefly summarizes the Ca(2+) homeostasis during early development of cardiomyocytes and reviews current knowledge of the regulatory mechanisms controlling Ca(2+) homeostasis during cardiomyocyte development.
Calcium ; physiology ; Calcium Channels ; metabolism ; physiology ; Calcium Signaling ; Heart ; embryology ; Homeostasis ; physiology ; Humans ; Intracellular Fluid ; physiology ; Myocytes, Cardiac ; metabolism ; physiology

Sixty years elapsed since Chang (Hsiang-Tung Chang, Xiang-Tong Zhang) presented his seminal report "Cortical neurons with particular reference to the apical dendrite" at the Cold Spring Harbor Symposium. Thanks to the development of elaborated techniques through the 6 decades, our understanding of the dendrite has been pushed forward greatly: the backward and forward conductions during excitation, sodium and calcium conductances, chemical excitation by uncaging glutamate at a dimension of micrometer, and the quantitative study of chemical organization of postsynaptic density (PSD), etc. Though the progression is great, there are still tough problems in dendritic research, especially the integration through dendritic spine.
Calcium Signaling ; Dendrites ; physiology ; Glutamic Acid ; metabolism

The purpose of this study is to identify the electrical activity of neuron, the existence of the transition from bursting pattern to spiking pattern and the ion mechanism of the bursting pattern. The intracellular electrical activity patterns of single neurons in the stomatogastric ganglion (STG) of crayfish were recorded when the extracellular calcium concentration ([Ca(2+)](o)) or calcium-dependent potassium channel blocker tetraethylammonium concentration ([TEA](o)) were changed, using intracellular recording method. These single neurons were also functionally isolated from the ganglion by application of atropine and picrotoxin which could block the inhibitory acetylcholine synapses and glutamatergic synapses respectively. When [Ca(2+)](o) was decreased by increasing EGTA, the membrane potential of the neuron was increased, and the electrical activity patterns were changed from the resting state with lower potential value (resting state of polarization) to the bursting pattern firstly, and then to the spiking pattern, at last to the resting state with higher potential value (resting state of depolarization). When [TEA](o) was increased, the membrane potential of the neuron was increased, and the electrical activity pattern was changed from the resting state with lower potential value (resting state of polarization) to the bursting pattern firstly, and then to the spiking pattern. The duration of the burst of the bursting pattern was increased. When [Ca(2+)](o) was increased or [TEA](o) was decreased, an inverse procedure of the electrical activity pattern was exhibited. On one hand, the results indicate that a single neuron can generate various electrical activity patterns corresponding to different physiological conditions, and the regularity of the transitions between different electrical activity patterns. On the other hand, the results identify that the initiation and termination of the burst in bursting pattern are determined by calcium-activated potassium conductance, which is adjusted by intracellular calcium concentration influenced by inward calcium current. It may be the ionic mechanism of generation of the bursting pattern in a single neuron.
Action Potentials ; physiology ; Animals ; Astacoidea ; physiology ; Calcium ; metabolism ; Calcium Channels ; metabolism ; Ganglia, Invertebrate ; physiology ; Neurons ; physiology ; Potassium Channels, Calcium-Activated ; metabolism

As an important intracellular messenger, Ca2+ plays a major role in sperm motility. In spermatozoa, multiple Ca2(+)-permeable channels have been identified in the plasma membrane of mammalian sperm, including voltage-gated Ca2+ channels (Cav channels), cyclic nucleotide-gated channels (CNGC), cation channels of sperm (CatSper) and the transient receptor potential (TRP) family. As calcium regulation of sperm motility is mainly mediated by these calcium channels, any aberration of the channels can lead to the decline of sperm activities. Recent progress in the researches on the relationship between sperm motility and calcium-related ion channels is briefly reviewed in this article.
Animals ; Calcium ; metabolism ; Calcium Channels ; Male ; Sperm Motility ; physiology ; Spermatozoa ; physiology

Cytosolic Ca(2+) ions play an important role in the regulation of numerous aspects of cellular activity in virtually all cell types. There is a complex interaction between the neuronal electrical signals on plasma membrane and the chemical signals of intracellular calcium. Each neuron can be considered as a binary membrane system with plasma membrane and endoplasmic reticulum membrane, and the neuronal endoplasmic reticulum can be regarded as a neuron-within-a-neuron. This review explores the simulation modeling of neuronal dynamics mutually coupled with the intracellular calcium signaling released from endoplasmic reticulum through the inositol 1,4,5-trisphosphate receptor calcium channels. We show that a current trend is to include the intracellular calcium dynamics into the neuronal models, and the frontier of this research is now shifting to spatial neuronal models with diffusing intracellular calcium. It is expected that more important results will be obtained with the neuronal models incorporating the intracellular calcium dynamics, especially the spatial models considering the calcium diffusion both in soma and dendritic branches.
Animals ; Calcium ; metabolism ; Calcium Signaling ; physiology ; Cytosol ; metabolism ; Endoplasmic Reticulum ; metabolism ; physiology ; Humans ; Inositol 1,4,5-Trisphosphate Receptors ; metabolism ; Models, Neurological ; Neurons ; metabolism ; physiology

OBJECTIVETo explore the dependence of Ca2+ on the acetylcholine (ACh)-sensitive potassium current in guinea pig type II vestibular hair cells.

METHODSUnder the whole-cell patch mode, the current amplitude of the ACh-sensitive potassium current was recorded in response to the concentration change of the extracellular or intracellular Ca2+.

RESULTSFollowing application of ACh, type II vestibular hair cells displayed the sustained potassium current, which was inhibited by tetraethylammonium chloride (TEA), but not inhibited by 4-aminopyrine (4-AP). The activation of the ACh-sensitive potassium current was strongly affected by the concentration of the extracellular Ca2+. The current amplitude of the ACh-sensitive potassium increased following the increase of Ca2+ concentration from 0 mmol/L to 4 mmol/L At the concentration of 4 mmol/L Ca2+, the current amplitude of the ACh-sensitive potassium current reached the maximal response. Lowering the Ca2 concentration in the external solution from 4 mmol/L to 0. 5 mmol/L, the current amplitude of the ACh-sensitive potassium current was inhibited to (36.5 +/- 6.5)%. However, no difference was found in the presence and in the absence of the intracellular heparin, which was a well-known blocker of the inositol trisphosphate-dependent calcium release channels. In addition, the calcium channel blocker, Cd2+, inhibited the ACh-sensitive potassium current.

CONCLUSIONSThe activation of the ACh-sensitive potassium current in guinea pig type II vestibular hair cells was dependent on the extracellular Ca2+ influx through the calcium channel. The application of ACh would stimulate membrane Ca2+ channels; the influx of Ca2+ will then activate the calcium-dependent potassium current in guinea pig type II hair cells to mediate the hyperpolarization effect.

Acetylcholine ; physiology ; Animals ; Calcium ; metabolism ; Calcium Channel Blockers ; metabolism ; Calcium Channels ; metabolism ; Guinea Pigs ; Hair Cells, Vestibular ; metabolism ; physiology ; Membrane Potentials ; Patch-Clamp Techniques

Contraction of smooth muscle cells is triggered by an increase in cytosolic Ca(2+) upon agonist stimulation. Ca(2+) influx across the plasma membrane constitutes a major component of the agonist-induced response in smooth muscle cells. Traditionally, voltage-operated Ca(2+) channel (VOCC) is considered as the channel mediating the Ca(2+) entry. However, this view has been challenged by recent discoveries, which demonstrated that other types of ion channels, such as store-operated and/or receptor-operated Ca(2+) channels (SOCC and/or ROCC), also participate in Ca(2+) response induced by agonists in smooth muscle cells. SOCC is defined as the channel activated in response to the depletion of the internal Ca(2+) stores, an event secondary to G protein coupled receptor or receptor tyrosine kinase stimulation. The Ca(2+) flow mediated by SOCC is termed as capacitative Ca(2+) entry (CCE). Previous study from other group has demonstrated that VOCC played a predominant role in ACh-induced contraction of distal colon smooth muscle in guinea pig. However, whether SOCC participates in the agonist-induced contractile response in this particular tissue is unknown. The present study was performed to investigate the role of CCE in ACh-induced mechanical activity of distal colon smooth muscle in rats. The contractile function of the smooth muscle was assessed by measuring isometric force of isolated rat distal colon rings. We showed that both high extracellular K(+) (40 mmol/L) and ACh (5 mumol/L) evoked striking contraction of the smooth muscle. The contractile responses were almost abolished by removal of extracellular Ca(2+) with ethylene glycol-bis(2-aminoethylether)-N,N,N',N' tetraacetic acid (EGTA), suggesting a critical contribution of extracellular source of Ca(2+) to the contraction. Verapamil (5 mumol/L), an L-type VOCC blocker, significantly attenuated, but didn't completely eliminate the high K(+)- and ACh-induced contraction (74% and 41% for high K(+) and ACh, respectively), indicating that additional channels might be involved in the contractile mechanism. Furthermore, ACh only induced transient contractions in the absence of extracellular Ca(2+). Readmission of Ca(2+) into the extracellular compartment resulted in a significant and sustained increase in the tension of the smooth muscle. This response was not affected by verapamil (5 mumol/L) and Cd(2+) (5 mumol/L), both of which efficiently block VOCC at the doses. However, La(3+), a known inhibitor of SOCC, significantly suppressed the Ca(2+) readdition-induced contraction in a dose-dependent manner. On the basis of these results, we conclude that contraction of smooth muscle in the distal colon is regulated by multiple Ca(2+) channels. In addition to VOCC-mediated Ca(2+) influx, SOCC-mediated CCE participates in agonist-induced contractile response of distal colon smooth muscle in rats.
Acetylcholine ; physiology ; Animals ; Calcium ; metabolism ; Calcium Channels ; physiology ; Colon ; physiology ; Female ; Male ; Muscle Contraction ; physiology ; Muscle, Smooth ; physiology ; Myocytes, Smooth Muscle ; physiology ; Rats ; Rats, Sprague-Dawley ; Verapamil ; pharmacology

The cyclic nucleotide-gated (CNG) channel is a nonselective cation channel and one of the main entrances of Ca2+ influxion into cells. CNG channels are opened by direct binding of cyclic nucleotides. Six different genes encode the CNG protein, 4 A subunits and 2 B subunits. The activity of CNG channels can be regulated by Ca2+/Ca(2+)-binding proteins (CaM) and phosphorylation/dephosphorylation. Recently, extensive attention has been drawn to the researches on CNG channels in the reproductive system, and many studies show that CNG channels play a pivotal role in sperm motility, capacitation and acrosome reaction. This article focuses on the relationship of CNG channels with sperm function.
Animals ; Calcium ; metabolism ; Cyclic Nucleotide-Gated Cation Channels ; physiology ; Humans ; Male ; Spermatozoa ; metabolism ; physiology

Mitochondria-associated endoplasmic reticulum membranes (MAMs) are the physical connection sites between mitochondria and endoplasmic reticulum (ER). As the compartments controlling substance and information communications between ER and mitochondria, MAMs were involved in the regulation of various pathophysiological processes, such as calcium homeostasis, mitochondrial morphology and function, lipid metabolism and autophagy. In the past decades, accumulating lines of evidence have revealed the pivotal role of MAMs in diverse cardiovascular diseases (CVD). Aging is one of the major independent risk factors for CVD, which causes progressive degeneration of the cardiovascular system, leading to increased morbidity and mortality of CVD. This review aims to summarize the research progress of MAMs in age-related CVD, and explore new targets for its prevention and treatment.
Humans ; Mitochondrial Membranes ; Cardiovascular Diseases/metabolism* ; Calcium Signaling/physiology* ; Mitochondria/physiology* ; Endoplasmic Reticulum/metabolism*

AIMThe characteristics of ryanodine receptor in rat cardiac sarcoplasmic reticulum (SR) and nuclear envelope (NE) were studied.

METHODSVelocity and isopyknic gradient centrifugation was employed to fractionate rat SR and NE. Ryanodine receptor was assayed with [3H] ryanodine saturate binding to the preparations.

RESULTSThe maximal binding (Bmax) and dissociating constant (Kd) of ryanodine receptor in rat cardiac NE were, 1.7% and 60% of those in SR respectively. Phosphorylation in vitro by PKA and PKC increased Bmax of the receptors in SR by 372% and 121%, and augmented those in NE by 221% and 306%, without any effects on Kd.

CONCLUSIONRyanodine receptors were present in rat myocardial NE, with lower density and higher affinity than those located in SR, which can be activated by PKA and PKC.

Animals ; Calcium ; metabolism ; Kinetics ; Myocardium ; metabolism ; Nuclear Envelope ; metabolism ; physiology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Ryanodine ; metabolism ; Ryanodine Receptor Calcium Release Channel ; metabolism ; Sarcoplasmic Reticulum ; metabolism ; physiology