Journal articles on the topic 'Calcium Wave'
To see the other types of publications on this topic, follow the link: Calcium Wave.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Calcium Wave.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Ishide, N., T. Urayama, K. Inoue, T. Komaru, and T. Takishima. "Propagation and collision characteristics of calcium waves in rat myocytes." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (September 1, 1990): H940—H950. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h940.
Full textAbstract:
In myocytes, local contractions occur spontaneously and propagate as traveling waves. We observed the waves in myocytes as local changes in fura-2 fluorescence and determined some characteristics of the wave. Myocytes were enzymatically isolated from rat left ventricles and incubated with 2 microM fura-2/AM for 60 min. Microscopic fluorescence images of myocytes were recorded with a high-sensitivity video camera. The images were digitally analyzed, frame by frame, and temporal changes in local fluorescence were displayed. With the excitation wavelength at 380 nm, the darker band propagates as the traveling wave. With the excitation wavelength at 340 nm, the wave appears brighter. With the isosbestic wavelength at 360 nm, the wave is not discernible. The waves are thus considered to be traveling waves of change in local cytoplasmic calcium ion concentration (calcium wave). Velocity, amplitude, and width of the calcium waves appeared to be fairly constant during their propagation. When two waves propagating in opposite directions collided, summation of the waves did not occur. After the collision both waves disappeared. These observations support the idea that the waves propagate by inducing calcium release from adjacent sarcoplasmic reticulum. Phenomena observed during the collision indicate that there is a refractory period after the calcium transient; spatially, a refractory zone exists in the wake of the wave.
2
Malhó, Rui, Ana Moutinho, Arnold van der Luit, and Anthony J. Trewavas. "Spatial characteristics to calcium signalling; the calcium wave as a basic unit in plant cell calcium signalling." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 353, no. 1374 (September 29, 1998): 1463–73. http://dx.doi.org/10.1098/rstb.1998.0302.
Full textAbstract:
Many signals that modify plant cell growth and development initiate changes in cytoplasmic Ca 2+ . The subsequent movement of Ca 2+ in the cytoplasm is thought to take place via waves of free Ca 2+ . These waves may be initiated at defined regions of the cell and movement requires release from a reticulated endoplasmic reticulum and the vacuole. The mechanism of wave propagation is outlined and the possible basis of repetitive reticulum wave formation, Ca 2+ oscillations and capacitative Ca 2+ signalling is discussed. Evidence for the presence of Ca 2+ waves in plant cells is outlined, and from studies on raphides it is suggested that the capabilities for capacitative Ca 2+ signalling are also present. The paper finishes with an outline of the possible interrelation between Ca 2+ waves and organelles and describes the intercellular movement of Ca 2+ waves and the relevance of such information communication to plant development.
3
Swann, Karl, Alex McDougall, and Michael Whitaker. "Calcium signalling at fertilization." Journal of the Marine Biological Association of the United Kingdom 74, no. 1 (February 1994): 3–16. http://dx.doi.org/10.1017/s002531540003561x.
Full textAbstract:
It is generally agreed that fertilization in deuterostomes is accompanied by a large intracellular calcium wave that triggers the onset of development, but we still do not know exactly how the calcium wave is generated. The question has two parts: how does interaction of sperm and egg initiate the calcium wave, and how does the calcium wave spread across the cell? Two provisional answers are available to the first part of the question, one involving receptor-G-protein interactions of the sort that mediate trans-membrane signal transduction in somatic cells, the other injection of an activating messenger when sperm and egg fuse. Both these ideas are being actively pursued; the dialectic is productive, albeit no synthesis is in sight. We discuss their strengths and weaknesses. The second part of the question can now be much more precisely formulated: thanks to the recent flush of interest in calcium waves in somatic cells, new ideas and new experimental tools are available. The work on somatic cells repays a debt to eggs, where the basic properties of calcium waves were first set out, ten years before they turned up in somatic cells.
4
KELLER, M., J. KAO, M. EGGER, and E. NIGGLI. "Calcium waves driven by “sensitization” wave-fronts." Cardiovascular Research 74, no. 1 (April 1, 2007): 39–45. http://dx.doi.org/10.1016/j.cardiores.2007.02.006.
Full text
5
Ishide, N., M. Miura, M. Sakurai, and T. Takishima. "Initiation and development of calcium waves in rat myocytes." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 2 (August 1, 1992): H327—H332. http://dx.doi.org/10.1152/ajpheart.1992.263.2.h327.
Full textAbstract:
To understand the characteristics of asynchrony in spontaneously occurring increases in cytoplasmic calcium concentrations ([Ca2+]i) in the cardiac myocyte, we observed newly developed changes in regional [Ca2+]i after a physical injury to the sarcolemma. Myocytes were isolated from rat left ventricle and loaded with acetoxymethyl ester of fura-2. We analyzed dynamic changes in fluorescence images by video densitometry. After the injury was imposed, three types of responses were observed: 1) rapid contracture with steady increase in [Ca2+]i; 2) periodic development of a calcium wave; and 3) quiescence after the injury. In some myocytes with the second type of response, a sustained burst of calcium waves was observed. In myocytes in which multiple calcium waves are present simultaneously, a propagated wave can reset a cycle of wave generation at the wave focus. Waves disappear after their collision, which indicates the existence of a refractory period after the calcium transient. The wave originating from the focus with the fastest frequency dominates the whole cell. Thus dynamic changes in regional [Ca2+]i are asynchronous but are organized by the following principles: 1) a regional increase in [Ca2+]i can propagate; 2) a propagated calcium wave can reset a cycle of wave initiation at the focus; and 3) a regional calcium transient leaves a refractory period.
6
Bowser, David N., and Baljit S. Khakh. "Vesicular ATP Is the Predominant Cause of Intercellular Calcium Waves in Astrocytes." Journal of General Physiology 129, no. 6 (May 15, 2007): 485–91. http://dx.doi.org/10.1085/jgp.200709780.
Full textAbstract:
Brain astrocytes signal to each other and neurons. They use changes in their intracellular calcium levels to trigger release of transmitters into the extracellular space. These can then activate receptors on other nearby astrocytes and trigger a propagated calcium wave that can travel several hundred micrometers over a timescale of seconds. A role for endogenous ATP in calcium wave propagation in hippocampal astrocytes has been suggested, but the mechanisms remain incompletely understood. Here we explored how calcium waves arise and directly tested whether endogenously released ATP contributes to astrocyte calcium wave propagation in hippocampal astrocytes. We find that vesicular ATP is the major, if not the sole, determinant of astrocyte calcium wave propagation over distances between ∼100 and 250 μm, and ∼15 s from the point of wave initiation. These actions of ATP are mediated by P2Y1 receptors. In contrast, metabotropic glutamate receptors and gap junctions do not contribute significantly to calcium wave propagation. Our data suggest that endogenous extracellular astrocytic ATP can signal over broad spatiotemporal scales.
7
Nihei, O. K., A. C. Campos de Carvalho, D. C. Spray, W. Savino, and L. A. Alves. "A novel form of cellular communication among thymic epithelial cells: intercellular calcium wave propagation." American Journal of Physiology-Cell Physiology 285, no. 5 (November 2003): C1304—C1313. http://dx.doi.org/10.1152/ajpcell.00568.2002.
Full textAbstract:
We here describe intercellular calcium waves as a novel form of cellular communication among thymic epithelial cells. We first characterized the mechanical induction of intercellular calcium waves in different thymic epithelial cell preparations: cortical 1-4C18 and medullary 3-10 thymic epithelial cell lines and primary cultures of thymic “nurse” cells. All thymic epithelial preparations responded with intercellular calcium wave propagation after mechanical stimulation. In general, the propagation efficacy of intercellular calcium waves in these cells was high, reaching 80-100% of the cells within a given confocal microscopic field, with a mean velocity of 6-10 μm/s and mean amplitude of 1.4- to 1.7-fold the basal calcium level. As evaluated by heptanol and suramin treatment, our results suggest the participation of both gap junctions and P2 receptors in the propagation of intercellular calcium waves in thymic nurse cells and the more prominent participation of gap junctions in thymic epithelial cell lines. Finally, in cocultures, the transmission of intercellular calcium wave was not observed between the mechanically stimulated thymic epithelial cell and adherent thymocytes, suggesting that intercellular calcium wave propagation is limited to thymic epithelial cells and does not affect the neighboring thymocytes. In conclusion, these data describe for the first time intercellular calcium waves in thymic epithelial cells and the participation of both gap junctions and P2 receptors in their propagation.
8
Jaffe, Lionel F. "Calcium waves." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1495 (January 11, 2008): 1311–17. http://dx.doi.org/10.1098/rstb.2007.2249.
Full textAbstract:
Waves through living systems are best characterized by their speeds at 20°C. These speeds vary from those of calcium action potentials to those of ultraslow ones which move at 1–10 and/or 10–20 nm s −1 . All such waves are known or inferred to be calcium waves. The two classes of calcium waves which include ones with important morphogenetic effects are slow waves that move at 0.2–2 μm s −1 and ultraslow ones. Both may be propagated by cycles in which the entry of calcium through the plasma membrane induces subsurface contraction. This contraction opens nearby stretch-sensitive calcium channels. Calcium entry through these channels propagates the calcium wave. Many slow waves are seen as waves of indentation. Some are considered to act via cellular peristalsis; for example, those which seem to drive the germ plasm to the vegetal pole of the Xenopus egg. Other good examples of morphogenetic slow waves are ones through fertilizing maize eggs, through developing barnacle eggs and through axolotl embryos during neural induction. Good examples of ultraslow morphogenetic waves are ones during inversion in developing Volvox embryos and across developing Drosophila eye discs. Morphogenetic waves may be best pursued by imaging their calcium with aequorins.
9
Huo, Bo, Xin L. Lu, and X. Edward Guo. "Intercellular calcium wave propagation in linear and circuit-like bone cell networks." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1912 (February 13, 2010): 617–33. http://dx.doi.org/10.1098/rsta.2009.0221.
Full textAbstract:
In the present study, the mechanism of intercellular calcium wave propagation in bone cell networks was identified. By using micro-contact printing and self-assembled monolayer technologies, two types of in vitro bone cell networks were constructed: open-ended linear chains and looped hexagonal networks with precisely controlled intercellular distances. Intracellular calcium responses of the cells were recorded and analysed when a single cell in the network was mechanically stimulated by nano-indentation. The looped cell network was shown to be more efficient than the linear pattern in transferring calcium signals from cell to cell. This phenomenon was further examined by pathway-inhibition studies. Intercellular calcium wave propagation was significantly impeded when extracellular adenosine triphosphate (ATP) in the medium was hydrolysed. Chemical uncoupling of gap junctions, however, did not significantly decrease the transferred distance of the calcium wave in the cell networks. Thus, it is extracellular ATP diffusion, rather than molecular transport through gap junctions, that dominantly mediates the transmission of mechanically elicited intercellular calcium waves in bone cells. The inhibition studies also demonstrated that the mechanical stimulation-induced calcium responses required extracellular calcium influx, whereas the ATP-elicited calcium wave relied on calcium release from the calcium store of the endoplasmic reticulum.
10
Whitaker, Michael. "Calcium at Fertilization and in Early Development." Physiological Reviews 86, no. 1 (January 2006): 25–88. http://dx.doi.org/10.1152/physrev.00023.2005.
Full textAbstract:
Fertilization calcium waves are introduced, and the evidence from which we can infer general mechanisms of these waves is presented. The two main classes of hypotheses put forward to explain the generation of the fertilization calcium wave are set out, and it is concluded that initiation of the fertilization calcium wave can be most generally explained in invertebrates by a mechanism in which an activating substance enters the egg from the sperm on sperm-egg fusion, activating the egg by stimulating phospholipase C activation through a src family kinase pathway and in mammals by the diffusion of a sperm-specific phospholipase C from sperm to egg on sperm-egg fusion. The fertilization calcium wave is then set into the context of cell cycle control, and the mechanism of repetitive calcium spiking in mammalian eggs is investigated. Evidence that calcium signals control cell division in early embryos is reviewed, and it is concluded that calcium signals are essential at all three stages of cell division in early embryos. Evidence that phosphoinositide signaling pathways control the resumption of meiosis during oocyte maturation is considered. It is concluded on balance that the evidence points to a need for phosphoinositide/calcium signaling during resumption of meiosis. Changes to the calcium signaling machinery occur during meiosis to enable the production of a calcium wave in the mature oocyte when it is fertilized; evidence that the shape and structure of the endoplasmic reticulum alters dynamically during maturation and after fertilization is reviewed, and the link between ER dynamics and the cytoskeleton is discussed. There is evidence that calcium signaling plays a key part in the development of patterning in early embryos. Morphogenesis in ascidian, frog, and zebrafish embryos is briefly described to provide the developmental context in which calcium signals act. Intracellular calcium waves that may play a role in axis formation in ascidian are discussed. Evidence that the Wingless/calcium signaling pathway is a strong ventralizing signal in Xenopus, mediated by phosphoinositide signaling, is adumbrated. The central role that calcium channels play in morphogenetic movements during gastrulation and in ectodermal and mesodermal gene expression during late gastrulation is demonstrated. Experiments in zebrafish provide a strong indication that calcium signals are essential for pattern formation and organogenesis.
11
Peti-Peterdi, János. "Calcium wave of tubuloglomerular feedback." American Journal of Physiology-Renal Physiology 291, no. 2 (August 2006): F473—F480. http://dx.doi.org/10.1152/ajprenal.00425.2005.
Full textAbstract:
ATP release from macula densa (MD) cells into the interstitium of the juxtaglomerular (JG) apparatus (JGA) is an integral component of the tubuloglomerular feedback (TGF) mechanism that controls the glomerular filtration rate. Because the cells of the JGA express a number of calcium-coupled purinergic receptors, these studies tested the hypothesis that TGF activation triggers a calcium wave that spreads from the MD toward distant cells of the JGA and glomerulus. Ratiometric calcium imaging of in vitro microperfused isolated JGA-glomerulus complex dissected from rabbits was performed with fluo-4/fura red and confocal fluorescence microscopy. Activation of TGF by increasing tubular flow rate at the MD rapidly produced a significant elevation in intracellular Ca2+ concentration ([Ca2+]i) in extraglomerular mesangial cells (by 187.6 ± 45.1 nM) and JG renin granular cells (by 281.4 ± 66.6 nM). Subsequently, cell-to-cell propagation of the calcium signal at a rate of 12.6 ± 1.1 μm/s was observed upstream toward proximal segments of the afferent arteriole and adjacent glomeruli, as well as toward intraglomerular elements including the most distant podocytes (5.9 ± 0.4 μm/s). The same calcium wave was observed in nonperfusing glomeruli, causing vasoconstriction and contractions of the glomerular tuft. Gap junction uncoupling, an ATP scavenger enzyme cocktail, and pharmacological inhibition of P2 purinergic receptors, but not adenosine A1 receptor blockade, abolished the changes in [Ca2+]i and propagation of the calcium wave. These studies provided evidence that both gap junctional communication and extracellular ATP are integral components of the TGF calcium wave.
12
Dumollard, R. "Calcium wave pacemakers in eggs." Journal of Cell Science 115, no. 18 (September 15, 2002): 3557–64. http://dx.doi.org/10.1242/jcs.00056.
Full text
13
Takeuchi, Yasuto, Rika Narumi, Ryutaro Akiyama, Elisa Vitiello, Takanobu Shirai, Nobuyuki Tanimura, Keisuke Kuromiya, et al. "Calcium Wave Promotes Cell Extrusion." Current Biology 30, no. 4 (February 2020): 670–81. http://dx.doi.org/10.1016/j.cub.2019.11.089.
Full text
14
Malysz, John, David Richardsons, Laura Farraway, Jan D. Huizinga, and Marie-Odile Christen. "Generation of slow wave type action potentials in the mouse small intestine involves a non-L-type calcium channel." Canadian Journal of Physiology and Pharmacology 73, no. 10 (October 1, 1995): 1502–11. http://dx.doi.org/10.1139/y95-208.
Full textAbstract:
Intrinsic electrical activities in various isolated segments of the mouse small intestine were recorded (i) to characterize action potential generation and (ii) to obtain a profile on the ion channels involved in initiating the slow wave type action potentials (slow waves). Gradients in slow wave frequency, resting membrane potential, and occurrence of spiking activity were found, with the proximal intestine exhibiting the highest frequency, the most hyperpolarized cell membrane, and the greatest occurrence of spikes. The slow waves were only partially sensitive to L-type calcium channel blockers. Nifedipine, verapamil, and pinaverium bromide abolished spikes that occurred on the plateau phase of the slow waves in all tissues. The activity that remained in the presence of L-type calcium channel blockers, the upstroke potential, retained a similar amplitude to the original slow wave and was of identical frequency. The upstroke potential was not sensitive to a reduction in extracellular chloride or to the sodium channel blockers tetrodotoxin and mexiletine. Abolishment of the Na+ gradient by removal of 120 mM extracellular Na+ reduced the upstroke potential frequency by 13–18% and its amplitude by 50–70% in the ileum. The amplitude was similarly reduced by Ni2+ (up to 5 mM), and by flufenamic acid (100 μM), a nonspecific cation and chloride channel blocker. Gadolinium, a nonspecific blocker of cation and stretch-activated channels, had no effect. Throughout these pharmacological manipulations, a robust oscillation remained at 5–10 mV. This oscillation likely reflects pacemaker activity. It was rapidly abolished by removal of extracellular calcium but not affected by L-type calcium channel blockers. In summary, the mouse small intestine has been established as a model for research into slow wave generation and electrical pacemaker activity. The upstroke part of the slow wave has two components, the pacemaker component involves a non-L-type calcium channel.Key words: slow wave, pacemaker, calcium channel, pinaverium, smooth muscle.
15
Kaneuchi, Taro, Caroline V. Sartain, Satomi Takeo, Vanessa L. Horner, Norene A. Buehner, Toshiro Aigaki, and Mariana F. Wolfner. "Calcium waves occur as Drosophila oocytes activate." Proceedings of the National Academy of Sciences 112, no. 3 (January 6, 2015): 791–96. http://dx.doi.org/10.1073/pnas.1420589112.
Full textAbstract:
Egg activation is the process by which a mature oocyte becomes capable of supporting embryo development. In vertebrates and echinoderms, activation is induced by fertilization. Molecules introduced into the egg by the sperm trigger progressive release of intracellular calcium stores in the oocyte. Calcium wave(s) spread through the oocyte and induce completion of meiosis, new macromolecular synthesis, and modification of the vitelline envelope to prevent polyspermy. However, arthropod eggs activate without fertilization: in the insects examined, eggs activate as they move through the female’s reproductive tract. Here, we show that a calcium wave is, nevertheless, characteristic of egg activation in Drosophila. This calcium rise requires influx of calcium from the external environment and is induced as the egg is ovulated. Pressure on the oocyte (or swelling by the oocyte) can induce a calcium rise through the action of mechanosensitive ion channels. Visualization of calcium fluxes in activating eggs in oviducts shows a wave of increased calcium initiating at one or both oocyte poles and spreading across the oocyte. In vitro, waves also spread inward from oocyte pole(s). Wave propagation requires the IP3 system. Thus, although a fertilizing sperm is not necessary for egg activation in Drosophila, the characteristic of increased cytosolic calcium levels spreading through the egg is conserved. Because many downstream signaling effectors are conserved in Drosophila, this system offers the unique perspective of egg activation events due solely to maternal components.
16
Sneyd, J., A. C. Charles, and M. J. Sanderson. "A model for the propagation of intercellular calcium waves." American Journal of Physiology-Cell Physiology 266, no. 1 (January 1, 1994): C293—C302. http://dx.doi.org/10.1152/ajpcell.1994.266.1.c293.
Full textAbstract:
In response to mechanical stimulation of a single cell, intercellular Ca2+ waves propagate through airway epithelial and glial cell cultures, providing a mechanism for intercellular communication. Experiments indicate that intercellular propagation of the Ca2+ wave is mediated by the movement of inositol 1,4,5-trisphosphate (IP3) through gap junctions. To explore the validity of this hypothesis, we have constructed and solved a system of partial differential equations that models the Ca2+ changes induced by the movement of IP3 between cells. The model is in good qualitative agreement with experimental data, including the behavior of the wave in the absence of extracellular Ca2+, the shape of the subsequent asynchronous Ca2+ oscillations, and the passage of a wave through a cell exhibiting Ca2+ oscillations. However, the concentration of IP3 that is required in each cell to propagate the wave may not be achieved by passive diffusion of IP3 through gap junctions from the stimulated cell. We therefore suggest that Ca(2+)-independent regenerative production of IP3 might be necessary for the propagation of intercellular Ca2+ waves.
17
Jørgensen, Niklas R., Steven T. Geist, Roberto Civitelli, and Thomas H. Steinberg. "ATP- and Gap Junction–dependent Intercellular Calcium Signaling in Osteoblastic Cells." Journal of Cell Biology 139, no. 2 (October 20, 1997): 497–506. http://dx.doi.org/10.1083/jcb.139.2.497.
Full textAbstract:
Many cells coordinate their activities by transmitting rises in intracellular calcium from cell to cell. In nonexcitable cells, there are currently two models for intercellular calcium wave propagation, both of which involve release of inositol trisphosphate (IP3)- sensitive intracellular calcium stores. In one model, IP3 traverses gap junctions and initiates the release of intracellular calcium stores in neighboring cells. Alternatively, calcium waves may be mediated not by gap junctional communication, but rather by autocrine activity of secreted ATP on P2 purinergic receptors. We studied mechanically induced calcium waves in two rat osteosarcoma cell lines that differ in the gap junction proteins they express, in their ability to pass microinjected dye from cell to cell, and in their expression of P2Y2 (P2U) purinergic receptors. ROS 17/2.8 cells, which express the gap junction protein connexin43 (Cx43), are well dye coupled, and lack P2U receptors, transmitted slow gap junction-dependent calcium waves that did not require release of intracellular calcium stores. UMR 106-01 cells predominantly express the gap junction protein connexin 45 (Cx45), are poorly dye coupled, and express P2U receptors; they propagated fast calcium waves that required release of intracellular calcium stores and activation of P2U purinergic receptors, but not gap junctional communication. ROS/P2U transfectants and UMR/Cx43 transfectants expressed both types of calcium waves. Gap junction–independent, ATP-dependent intercellular calcium waves were also seen in hamster tracheal epithelia cells. These studies demonstrate that activation of P2U purinergic receptors can propagate intercellular calcium, and describe a novel Cx43-dependent mechanism for calcium wave propagation that does not require release of intracellular calcium stores by IP3. These studies suggest that gap junction communication mediated by either Cx43 or Cx45 does not allow passage of IP3 well enough to elicit release of intracellular calcium stores in neighboring cells.
18
McDougall, Alex, Isabelle Gillot, and Michael Whitaker. "Thimerosal reveals calcium-induced calcium release in unfertilised sea urchin eggs." Zygote 1, no. 1 (February 1993): 35–42. http://dx.doi.org/10.1017/s0967199400001271.
Full textAbstract:
SummaryThe fertilisation calcium wave in sea urchin eggs triggers the onset of development. The wave is an explosive increase in intracellular free calcium concentration that begins at the point of sperm entry and crosses the egg in about 20 s. Thimerosal is a sulphydryl reagent that sensitises calcium release from intracellular stores in a variety of cell types. Treatment of unfertilised eggs with thimerosal causes a slow increase that results eventually in a large, spontaneous calcium transient and egg activation. At shorter times after thimerosal treatment, egg activation and the calcium transient can be triggered by calcium influx through voltage-gated calcium channels, a form of calcium-induced/calcium release (CICR). Thimerosal treatment also reduces the latency of the fertilisation calcium response and increases the velocity of the fertilisation wave. These results indicate that thimerosal can unmask CICR in sea urchin eggs and suggest that the ryanodine receptor channel based CICR may contribute to explosive calcium release during the fertilisation wave.
19
Seppey, Dominique, Roger Sauser, Michèle Koenigsberger, Jean-Louis Bény, and Jean-Jacques Meister. "Intercellular calcium waves are associated with the propagation of vasomotion along arterial strips." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H488—H496. http://dx.doi.org/10.1152/ajpheart.00281.2009.
Full textAbstract:
Vasomotion consists of cyclic arterial diameter variations induced by synchronous contractions and relaxations of smooth muscle cells. However, the arteries do not contract simultaneously on macroscopic distances, and a propagation of the contraction can be observed. In the present study, our aim was to investigate this propagation. We stimulated endothelium-denuded rat mesenteric arterial strips with phenylephrine (PE) to obtain vasomotion and observed that the contraction waves are linked to intercellular calcium waves. A velocity of ∼100 μm/s was measured for the two kinds of waves. To investigate the calcium wave propagation mechanisms, we used a method allowing a PE stimulation of a small area of the strip. No calcium propagation could be induced by this local stimulation when the strip was in its resting state. However, if a low PE concentration was added on the whole strip, local PE stimulations induced calcium waves, spreading over finite distances. The calcium wave velocity induced by local stimulation was identical to the velocity observed during vasomotion. This suggests that the propagation mechanisms are similar in the two cases. Using inhibitors of gap junctions and of voltage-operated calcium channels, we showed that the locally induced calcium propagation likely depends on the propagation of the smooth muscle cell depolarization. Finally, we proposed a model of the propagation mechanisms underlying these intercellular calcium waves.
20
Belyayev, Yu N., E. I. Yashin, and O. Y. Yashina. "Conversion of Elastic Wave Polarization in Calcium Molybdate Layer." Solid State Phenomena 284 (October 2018): 95–100. http://dx.doi.org/10.4028/www.scientific.net/ssp.284.95.
Full textAbstract:
Scattering of elastic waves in calcium molybdate films is considered. The transformation of elastic waves as a result of six-beam diffraction in an anisotropic layer is analyzed. This analysis is based on the transfer matrix method. The distribution of incident wave energy between six scattered waves is characterized by conversion coefficients. The method for conversion coefficients calculations is presented. It does not require solving algebraic problem on eigenvalues for waves in an anisotropic layer. Features of dependencies of conversion coefficients of CaMoO4 layers on angles of incidence, frequency and the thickness of the layer are demonstrated.
21
Sneyd, James, Steven Girard, and David Clapham. "Calcium wave propagation by calcium-induced calcium release: An unusual excitable system." Bulletin of Mathematical Biology 55, no. 2 (March 1993): 315–44. http://dx.doi.org/10.1007/bf02460886.
Full text
22
SNEYD, J., S. GIRARD, and D. CLAPHAM. "Calcium wave propagation by calcium-induced calcium release: An unusual excitable system." Bulletin of Mathematical Biology 55, no. 2 (March 1993): 315–44. http://dx.doi.org/10.1016/s0092-8240(05)80268-x.
Full text
23
Cheng, H., M. R. Lederer, W. J. Lederer, and M. B. Cannell. "Calcium sparks and [Ca2+]i waves in cardiac myocytes." American Journal of Physiology-Cell Physiology 270, no. 1 (January 1, 1996): C148—C159. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c148.
Full textAbstract:
Local elevations in intracellular calcium ("Ca2+ sparks") in heart muscle are elementary sarcoplasmic reticulum (SR) Ca(2+)-release events. Ca2+ sparks occur at a low rate in quiescent cells but can also be evoked by electrical stimulation of the cell to produce the cell-wide Ca2+ transient. In this study we investigate how Ca2+ sparks are related to propagating waves of elevated cytosolic Ca2+ induced by "Ca2+ overload." Single ventricular myocytes from rat were loaded with the Ca(2+)-sensitive indicator fluo 3 and imaged with a confocal microscope. After extracellular Ca2+ concentration was increased from 1 to 10 mM to produce Ca2+ overload, the frequency of spontaneous Ca2+ sparks, which occur at the t tubule/SR junction, increased approximately 4-fold, whereas the spark amplitude and spatial size increased 4.1-and 1.7-fold, respectively. In addition, a spectrum of larger subcellular events, including propagating Ca2+ waves, was observed. Ca2+ sparks were seen to occur at the majority (65%) of the sites of wave initiation. For slowly propagating Ca2+ waves, discrete Ca(2+)-release events, similar to Ca2+ sparks, were detected in the wave front. These Ca2+ sparks appeared to recruit other sparks along the wave front so that the wave progressed in a saltatory manner. We conclude that Ca2+ sparks are elementary events that can explain both the initiation and propagation of Ca2+ waves. In addition, we show that Ca2+ waves and electrically evoked Ca2+ transients have the same time course and interact with each other in a manner that is consistent with both phenomena having the same underlying mechanism(s). These results suggest that SR Ca2+ release during Ca2+ waves, like that during normal excitation-contraction coupling, results from the spatial and temporal summation of Ca2+ sparks.
24
Power, John M., and Pankaj Sah. "Dendritic spine heterogeneity and calcium dynamics in basolateral amygdala principal neurons." Journal of Neurophysiology 112, no. 7 (October 1, 2014): 1616–27. http://dx.doi.org/10.1152/jn.00770.2013.
Full textAbstract:
Glutamatergic synapses on pyramidal neurons are formed on dendritic spines where glutamate activates ionotropic receptors, and calcium influx via N-methyl-d-aspartate receptors leads to a localized rise in spine calcium that is critical for the induction of synaptic plasticity. In the basolateral amygdala, activation of metabotropic receptors is also required for synaptic plasticity and amygdala-dependent learning. Here, using acute brain slices from rats, we show that, in basolateral amygdala principal neurons, high-frequency synaptic stimulation activates metabotropic glutamate receptors and raises spine calcium by releasing calcium from inositol trisphosphate-sensitive calcium stores. This spine calcium release is unevenly distributed, being present in proximal spines, but largely absent in more distal spines. Activation of metabotropic receptors also generated calcium waves that differentially invaded spines as they propagated toward the soma. Dendritic wave invasion was dependent on diffusional coupling between the spine and parent dendrite which was determined by spine neck length, with waves preferentially invading spines with short necks. Spine calcium is a critical trigger for the induction of synaptic plasticity, and our findings suggest that calcium release from inositol trisphosphate-sensitive calcium stores may modulate homosynaptic plasticity through store-release in the spine head, and heterosynaptic plasticity of unstimulated inputs via dendritic calcium wave invasion of the spine head.
25
Cornell-Bell, A. H., R. M. Villalba, R. H. Selinfreund, B. D. Stein, J. L. Cornell, and L. A. Riblet. "Time-lapse confocal calcium imaging in an intact unrolled hippocampus preparation." Proceedings, annual meeting, Electron Microscopy Society of America 53 (August 13, 1995): 808–9. http://dx.doi.org/10.1017/s0424820100140415.
Full textAbstract:
The excitatory neurotransmitter glutamate (100 μM) induces intracellular calcium transients in cultured hippocampal astrocytes that can be imaged using the calcium indicator (Fluo3AM) and time-lapse microscopy. In response to glutamate (Fig. 1A), cultured astrocytes exhibit distinct patterns of intracellular Ca2+ oscillations and long-distance intercellular waves. Two distinct types of intercellular Ca2+ waves are attributed to excitation by different agonists of the glutamate receptor subtypes. A long-distance regenerative intercellular wave is induced by the ionotropic glutamate receptor, kainate (Fig. 1B). This is a true wave lasting for 50-125 sec with a constant velocity of 10-20 μm/sec. This wave requires extracellular Ca2+ and Na+ and is driven by the Na+/Ca2+ exchanger. A fast Ca2+ wave which travels at speeds from 10 to 200 μm/sec is dependent upon the metabotropic glutamate receptor, is inducible by t-ACPD and is dependent upon cytoplasmic release of Ca2+ regulated by IP3 (Fig. 1C). This wave is not dependent upon extracellular Ca2+ and is stopped by MCPG, a specific inhibitor of IP3-mediated intracellular Ca2+ release.
26
Lammers, Wim J. E. P., and John R. Slack. "Of Slow Waves and Spike Patches." Physiology 16, no. 3 (June 2001): 138–44. http://dx.doi.org/10.1152/physiologyonline.2001.16.3.138.
Full textAbstract:
In the small intestines, the major task of the slow wave is to induce mechanical movements in the intestinal wall by generating local calcium spikes. High resolution electrical mapping reveals fundamental differences in propagation between slow waves and calcium spikes. These differences suggest that slow waves and spikes are propagated by different mechanisms through different cell networks.
27
Matsui, Takaaki. "Calcium wave propagation during cell extrusion." Current Opinion in Cell Biology 76 (June 2022): 102083. http://dx.doi.org/10.1016/j.ceb.2022.102083.
Full text
28
Matsui, Takaaki. "Calcium wave propagation during cell extrusion." Current Opinion in Cell Biology 76 (June 2022): 102083. http://dx.doi.org/10.1016/j.ceb.2022.102083.
Full text
29
MIYAZAKI, SHUN-ICHI. "Calcium Wave in Activating Hamster Eggs." Biological Bulletin 176, no. 2S (April 1989): 21–24. http://dx.doi.org/10.2307/1541643.
Full text
30
Bazargani, Narges, and David Attwell. "Astrocyte calcium signaling: the third wave." Nature Neuroscience 19, no. 2 (January 27, 2016): 182–89. http://dx.doi.org/10.1038/nn.4201.
Full text
31
Parkash, Jai, and Kamlesh Asotra. "Calcium wave signaling in cancer cells." Life Sciences 87, no. 19-22 (November 2010): 587–95. http://dx.doi.org/10.1016/j.lfs.2010.09.013.
Full text
32
Bellinger, Steve. "Modeling calcium wave oscillations in astrocytes." Neurocomputing 65-66 (June 2005): 843–50. http://dx.doi.org/10.1016/j.neucom.2004.10.081.
Full text
33
Kusters, J. M. A. M., W. P. M. van Meerwijk, D. L. Ypey, A. P. R. Theuvenet, and C. C. A. M. Gielen. "Fast calcium wave propagation mediated by electrically conducted excitation and boosted by CICR." American Journal of Physiology-Cell Physiology 294, no. 4 (April 2008): C917—C930. http://dx.doi.org/10.1152/ajpcell.00181.2007.
Full textAbstract:
We have investigated synchronization and propagation of calcium oscillations, mediated by gap junctional excitation transmission. For that purpose we used an experimentally based model of normal rat kidney (NRK) cells, electrically coupled in a one-dimensional configuration (linear strand). Fibroblasts such as NRK cells can form an excitable syncytium and generate spontaneous inositol 1,4,5-trisphosphate (IP3)-mediated intracellular calcium waves, which may spread over a monolayer culture in a coordinated fashion. An intracellular calcium oscillation in a pacemaker cell causes a membrane depolarization from within that cell via calcium-activated chloride channels, leading to an L-type calcium channel-based action potential (AP) in that cell. This AP is then transmitted to the electrically connected neighbor cell, and the calcium inflow during that transmitted AP triggers a calcium wave in that neighbor cell by opening of IP3 receptor channels, causing calcium-induced calcium release (CICR). In this way the calcium wave of the pacemaker cell is rapidly propagated by the electrically transmitted AP. Propagation of APs in a strand of cells depends on the number of terminal pacemaker cells, the L-type calcium conductance of the cells, and the electrical coupling between the cells. Our results show that the coupling between IP3-mediated calcium oscillations and AP firing provides a robust mechanism for fast propagation of activity across a network of cells, which is representative for many other cell types such as gastrointestinal cells, urethral cells, and pacemaker cells in the heart.
34
Speksnijder, J. E., C. Sardet, and L. F. Jaffe. "The activation wave of calcium in the ascidian egg and its role in ooplasmic segregation." Journal of Cell Biology 110, no. 5 (May 1, 1990): 1589–98. http://dx.doi.org/10.1083/jcb.110.5.1589.
Full textAbstract:
We have studied egg activation and ooplasmic segregation in the ascidian Phallusia mammillata using an imaging system that let us simultaneously monitor egg morphology and calcium-dependent aequorin luminescence. After insemination, a wave of highly elevated free calcium crosses the egg with a peak velocity of 8-9 microns/s. A similar wave is seen in egg fertilized in the absence of external calcium. Artificial activation via incubation with WGA also results in a calcium wave, albeit with different temporal and spatial characteristics than in sperm-activated eggs. In eggs in which movement of the sperm nucleus after entry is blocked with cytochalasin D, the sperm aster is formed at the site where the calcium wave had previously started. This indicates that the calcium wave starts where the sperm enters. In 70% of the eggs, the calcium wave starts in the animal hemisphere, which confirms previous observations that there is a preference for sperm to enter this part of the egg (Speksnijder, J. E., L. F. Jaffe, and C. Sardet. 1989. Dev. Biol. 133:180-184). About 30-40 s after the calcium wave starts, a slower (1.4 microns/s) wave of cortical contraction starts near the animal pole. It carries the subcortical cytoplasm to a contraction pole, which forms away from the side of sperm entry and up to 50 degrees away from the vegetal pole. We propose that the point of sperm entry may affect the direction of ooplasmic segregation by causing it to tilt away from the vegetal pole, presumably via some action of the calcium wave.
35
Dumollard, Rémi, and Christian Sardet. "Three different calcium wave pacemakers in ascidian eggs." Journal of Cell Science 114, no. 13 (July 1, 2001): 2471–81. http://dx.doi.org/10.1242/jcs.114.13.2471.
Full textAbstract:
Calcium wave pacemakers in fertilized eggs of ascidians and mouse are associated with accumulations of cortical endoplasmic reticulum in the vegetal hemisphere. In ascidians, two distinct pacemakers (PM1 and PM2) generate two series of calcium waves necessary to drive meiosis I and II. Pacemaker PM2 is stably localized in a cortical ER accumulation situated in the vegetal contraction pole. We now find that pacemaker PM1 is situated in a cortical ER-rich domain that forms around the sperm aster and moves with it during the calcium-dependant cortical contraction triggered by the fertilizing sperm. Global elevations of inositol (1,4,5)-trisphosphate (Ins(1,4,5)P3) levels produced by caged Ins(1,4,5)P3 or caged glycero-myo-PtdIns(4,5)P2 photolysis reveal that the cortex of the animal hemisphere, also rich in ER-clusters, is the cellular region most sensitive to Ins(1,4,5)P3 and acts as a third type of pacemaker (PM3). Surprisingly, the artificial pacemaker PM3 predominates over the natural pacemaker PM2, located at the opposite pole. Microtubule depolymerization does not alter the activity nor the location of the three pacemakers. By contrast, blocking the acto-myosin driven cortical contraction with cytochalasin B prevents PM1 migration and inhibits PM2 activity. PM3, however, is insensitive to cytochalasin B. Our experiments suggest that the three distinct calcium wave pacemakers are probably regulated by different spatiotemporal variations in Ins(1,4,5)P3 concentration. In particular, the activity of the natural calcium wave pacemakers PM1 and PM2 depends on the apposition of a cortical ER-rich domain to a source of Ins(1,4,5)P3 production in the cortex. Movies available on-line
36
Mathiesen, Claus, Alexey Brazhe, Kirsten Thomsen, and Martin Lauritzen. "Spontaneous Calcium Waves in Bergman Glia Increase with Age and Hypoxia and may Reduce Tissue Oxygen." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (December 5, 2012): 161–69. http://dx.doi.org/10.1038/jcbfm.2012.175.
Full textAbstract:
Glial calcium (Ca2+) waves constitute a means to spread signals between glial cells and to neighboring neurons and blood vessels. These waves occur spontaneously in Bergmann glia (BG) of the mouse cerebellar cortex in vivo. Here, we tested three hypotheses: (1) aging and reduced blood oxygen saturation alters wave activity; (2) glial Ca2+ waves change cerebral oxygen metabolism; and (3) neuronal and glial wave activity is correlated. We used two-photon microscopy in the cerebellar cortexes of adult (8- to 15-week-old) and aging (48- to 80-week-old) ketamine-anesthetized mice after bolus loading with OGB-1/AM and SR101. We report that the occurrence of spontaneous waves is 20 times more frequent in the cerebellar cortex of aging as compared with adult mice, which correlated with a reduction in resting brain oxygen tension. In adult mice, spontaneous glial wave activity increased on reducing resting brain oxygen tension, and ATP-evoked glial waves reduced the tissue O2 tension. Finally, although spontaneous Purkinje cell (PC) activity was not associated with increased glia wave activity, spontaneous glial waves did affect intracellular Ca2+ activity in PCs. The increased wave activity during aging, as well as low resting brain oxygen tension, suggests a relationship between glial waves, brain energy homeostasis, and pathology.
37
Muto, A., S. Kume, T. Inoue, H. Okano, and K. Mikoshiba. "Calcium waves along the cleavage furrows in cleavage-stage Xenopus embryos and its inhibition by heparin." Journal of Cell Biology 135, no. 1 (October 1, 1996): 181–90. http://dx.doi.org/10.1083/jcb.135.1.181.
Full textAbstract:
Calcium signaling is known to be associated with cytokinesis; however, the detailed spatio-temporal pattern of calcium dynamics has remained unclear. We have studied changes of intracellular free calcium in cleavage-stage Xenopus embryos using fluorescent calcium indicator dyes, mainly Calcium Green-1. Cleavage formation was followed by calcium transients that localized to cleavage furrows and propagated along the furrows as calcium waves. The calcium transients at the cleavage furrows were observed at each cleavage furrow at least until blastula stage. The velocity of the calcium waves at the first cleavage furrow was approximately 3 microns/s, which was much slower than that associated with fertilization/egg activation. These calcium waves traveled only along the cleavage furrows and not in the direction orthogonal to the furrows. These observations imply that there exists an intracellular calcium-releasing activity specifically associated with cleavage furrows. The calcium waves occurred in the absence of extracellular calcium and were inhibited in embryos injected with heparin an inositol 1,4,5-trisphosphate (InsP3) receptor antagonist. These results suggest that InsP3 receptor-mediated calcium mobilization plays an essential role in calcium wave formation at the cleavage furrows.
38
Malysz, John, Graeme Donnelly, and Jan D. Huizinga. "Regulation of slow wave frequency by IP3-sensitive calcium release in the murine small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (March 1, 2001): G439—G448. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g439.
Full textAbstract:
Slow waves determine frequency and propagation characteristics of contractions in the small intestine, yet little is known about mechanisms of slow wave regulation. We propose a role for intracellular Ca2+, inositol 1,4,5,-trisphosphate (IP3)-sensitive Ca2+ release, and sarcoplasmic reticulum (SR) Ca2+ content in the regulation of slow wave frequency because 1) 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid-AM, a cytosolic Ca2+ chelator, reduced the frequency or abolished the slow waves; 2) thapsigargin and cyclopiazonic acid (CPA), inhibitors of SR Ca2+-ATPase, decreased slow wave frequency; 3) xestospongin C, a reversible, membrane-permeable blocker of IP3-induced Ca2+release, abolished slow wave activity; 4) caffeine and phospholipase C inhibitors (U-73122, neomycin, and 2-nitro-4-carboxyphenyl- N, N-diphenylcarbamate) inhibited slow wave frequency; 5) in the presence of CPA or thapsigargin, stimulation of IP3 synthesis with carbachol, norepinephrine, or phenylephrine acting on α1-adrenoceptors initially increased slow wave frequency but thereafter increased the rate of frequency decline, 6) thimerosal, a sensitizing agent of IP3 receptors increased slow wave frequency, and 7) ryanodine, a selective modulator of Ca2+-induced Ca2+ release, had no effect on slow wave frequency. In summary, these data are consistent with a role of IP3-sensitive Ca2+ release and the rate of SR Ca2+ refilling in regulation of intestinal slow wave frequency.
39
Swann, K., and M. Whitaker. "The part played by inositol trisphosphate and calcium in the propagation of the fertilization wave in sea urchin eggs." Journal of Cell Biology 103, no. 6 (December 1, 1986): 2333–42. http://dx.doi.org/10.1083/jcb.103.6.2333.
Full textAbstract:
Sea urchin egg activation at fertilization is progressive, beginning at the point of sperm entry and moving across the egg with a velocity of 5 microns/s. This activation wave (Kacser, H., 1955, J. Exp. Biol., 32:451-467) has been suggested to be the result of a progressive release of calcium from a store within the egg cytoplasm (Jaffe, L. F., 1983, Dev. Biol., 99:265-276). The progressive release of calcium may be due to the production of inositol trisphosphate (InsP3), a second messenger. We show here that a wave of calcium release crosses the Lytechinus pictus egg; the peak of the wave travels with a velocity of 5 microns/s; microinjection of InsP3 causes the release of calcium within the egg; calcium release (as judged by fertilization envelope elevation) is abolished by prior injection of the calcium chelator EGTA; neomycin, an inhibitor of InsP3 production, does not prevent the release of calcium in response to InsP3 but does abolish the wave of calcium release; the egg cytoplasm rapidly buffers microinjected calcium; the calcium concentration required to cause fertilization membrane elevation when microinjected is very similar to that required to stimulate the production of InsP3 in vitro; and the progressive fertilization membrane elevation seen after microinjection of calcium buffers appears to be due to diffusion of the buffer across the egg cytoplasm rather than to the induction of the activation wave. We conclude that InsP3 diffuses through the egg cytoplasm much more readily than calcium ions and that calcium-stimulated production of InsP3 and InsP3-induced calcium release from an internal store can account for the progressive release of calcium at fertilization.
40
Straub, Stephen V., David R. Giovannucci, and David I. Yule. "Calcium Wave Propagation in Pancreatic Acinar Cells." Journal of General Physiology 116, no. 4 (September 25, 2000): 547–60. http://dx.doi.org/10.1085/jgp.116.4.547.
Full textAbstract:
In pancreatic acinar cells, inositol 1,4,5-trisphosphate (InsP3)–dependent cytosolic calcium ([Ca2+]i) increases resulting from agonist stimulation are initiated in an apical “trigger zone,” where the vast majority of InsP3 receptors (InsP3R) are localized. At threshold stimulation, [Ca2+]i signals are confined to this region, whereas at concentrations of agonists that optimally evoke secretion, a global Ca2+ wave results. Simple diffusion of Ca2+ from the trigger zone is unlikely to account for a global [Ca2+]i elevation. Furthermore, mitochondrial import has been reported to limit Ca2+ diffusion from the trigger zone. As such, there is no consensus as to how local [Ca2+]i signals become global responses. This study therefore investigated the mechanism responsible for these events. Agonist-evoked [Ca2+]i oscillations were converted to sustained [Ca2+]i increases after inhibition of mitochondrial Ca2+ import. These [Ca2+]i increases were dependent on Ca2+ release from the endoplasmic reticulum and were blocked by 100 μM ryanodine. Similarly, “uncaging” of physiological [Ca2+]i levels in whole-cell patch-clamped cells resulted in rapid activation of a Ca2+-activated current, the recovery of which was prolonged by inhibition of mitochondrial import. This effect was also abolished by ryanodine receptor (RyR) blockade. Photolysis of d-myo InsP3 P4(5)-1-(2-nitrophenyl)-ethyl ester (caged InsP3) produced either apically localized or global [Ca2+]i increases in a dose-dependent manner, as visualized by digital imaging. Mitochondrial inhibition permitted apically localized increases to propagate throughout the cell as a wave, but this propagation was inhibited by ryanodine and was not seen for minimal control responses resembling [Ca2+]i puffs. Global [Ca2+]i rises initiated by InsP3 were also reduced by ryanodine, limiting the increase to a region slightly larger than the trigger zone. These data suggest that, while Ca2+ release is initially triggered through InsP3R, release by RyRs is the dominant mechanism for propagating global waves. In addition, mitochondrial Ca2+ import controls the spread of Ca2+ throughout acinar cells by modulating RyR activation.
41
Petrovič, Pavol, Ivan Valent, Elena Cocherová, Jana Pavelková, and Alexandra Zahradníková. "Ryanodine receptor gating controls generation of diastolic calcium waves in cardiac myocytes." Journal of General Physiology 145, no. 6 (May 25, 2015): 489–511. http://dx.doi.org/10.1085/jgp.201411281.
Full textAbstract:
The role of cardiac ryanodine receptor (RyR) gating in the initiation and propagation of calcium waves was investigated using a mathematical model comprising a stochastic description of RyR gating and a deterministic description of calcium diffusion and sequestration. We used a one-dimensional array of equidistantly spaced RyR clusters, representing the confocal scanning line, to simulate the formation of calcium sparks. Our model provided an excellent description of the calcium dependence of the frequency of diastolic calcium sparks and of the increased tendency for the production of calcium waves after a decrease in cytosolic calcium buffering. We developed a hypothesis relating changes in the propensity to form calcium waves to changes of RyR gating and tested it by simulation. With a realistic RyR gating model, increased ability of RyR to be activated by Ca2+ strongly increased the propensity for generation of calcium waves at low (0.05–0.1-µM) calcium concentrations but only slightly at high (0.2–0.4-µM) calcium concentrations. Changes in RyR gating altered calcium wave formation by changing the calcium sensitivity of spontaneous calcium spark activation and/or the average number of open RyRs in spontaneous calcium sparks. Gating changes that did not affect RyR activation by Ca2+ had only a weak effect on the propensity to form calcium waves, even if they strongly increased calcium spark frequency. Calcium waves induced by modulating the properties of the RyR activation site could be suppressed by inhibiting the spontaneous opening of the RyR. These data can explain the increased tendency for production of calcium waves under conditions when RyR gating is altered in cardiac diseases.
42
Lee, Cheng-Han, Kuo-Hsing Kuo, Jiazhen Dai, and Cornelis van Breemen. "Asynchronous calcium waves in smooth muscle cells." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (August 1, 2005): 733–41. http://dx.doi.org/10.1139/y05-083.
Full textAbstract:
Asynchronous Ca2+ waves or wave-like [Ca2+]i oscillations constitute a specialized form of agonist-induced Ca2+ signaling that is observed in a variety of smooth muscle cell types. Functionally, it is involved in the contractile regulation of the smooth muscle cells as it signals for tonic contraction in certain smooth muscle cells while causing relaxation in others. Mechanistically, repetitive Ca2+ waves are produced by repetitive cycles of sarcoplasmic reticulum Ca2+ release followed by Ca2+ uptake. Plasmalemmal Ca2+ entry mechanisms are important for providing the additional Ca2+ necessary to maintain proper refilling of the sarcoplasmic reticulum Ca2+ store and support ongoing Ca2+ waves. In this paper, we will review the phenomenon of asynchronous Ca2+ waves in smooth muscle and discuss the scientific and clinical significance of this new understanding.Key words: excitation-contraction coupling, confocal fluoresence microscopy, calcium signaling.
43
Jaffe, Lionel F., and Robbert Créton. "On the conservation of calcium wave speeds." Cell Calcium 24, no. 1 (July 1998): 1–8. http://dx.doi.org/10.1016/s0143-4160(98)90083-5.
Full text
44
Kupferman, R., P. P. Mitra, P. C. Hohenberg, and S. S. Wang. "Analytical calculation of intracellular calcium wave characteristics." Biophysical Journal 72, no. 6 (June 1997): 2430–44. http://dx.doi.org/10.1016/s0006-3495(97)78888-x.
Full text
45
Tordjmann, Thierry, Laurent Combettes, and Michel Claret. "Nitric Oxide as a Calcium Wave Accelerator." Hepatology 32, no. 1 (December 30, 2003): 156–57. http://dx.doi.org/10.1002/hep.510320126.
Full text
46
Eem, Changkyoung, Hyunki Hong, and Yoohun Noh. "Deep-Learning Model to Predict Coronary Artery Calcium Scores in Humans from Electrocardiogram Data." Applied Sciences 10, no. 23 (December 7, 2020): 8746. http://dx.doi.org/10.3390/app10238746.
Full textAbstract:
We introduce a deep-learning neural network model that uses electrocardiogram (ECG) data to predict coronary artery calcium scores, which can be useful for reliably detecting cardiovascular risk in patients. In our pre-processing method, each lead of the ECG is segmented into several waves with an interval, which is determined as the period from the starting point of a P-wave to the end point of a T-wave. The number of segmented waves of one lead represents the number of heartbeats of the subject per 10 s. The segmented waves of one cycle are transformed into normalized waves with an amplitude of 0–1. Owing to the use of eight-lead ECG waves, the input ECG dataset has two dimensions. We used a convolutional neural network with 16 layers and 5 fully connected layers, comprising a one-dimensional filter to examine the normalized wave of one lead, rather than a two-dimensional filter to examine the coherence among the unit waves of eight leads. The training and testing are repeated 10 times with a randomly assigned dataset (177,547 ECGs). Our network model achieves an average area under the receiver operating characteristic curve of 0.801–0.890, and the average accuracy is in the range of 72.9–80.6%.
47
Sneyd, J., B. T. Wetton, A. C. Charles, and M. J. Sanderson. "Intercellular calcium waves mediated by diffusion of inositol trisphosphate: a two-dimensional model." American Journal of Physiology-Cell Physiology 268, no. 6 (June 1, 1995): C1537—C1545. http://dx.doi.org/10.1152/ajpcell.1995.268.6.c1537.
Full textAbstract:
In response to mechanical stimulation of a single cell, airway epithelial cells in culture exhibit a wave of increased intracellular free Ca2+ concentration that spreads from cell to cell over a limited distance through the culture. We present a detailed analysis of the intercellular wave in a two-dimensional sheet of cells. The model is based on the hypothesis that the wave is the result of diffusion of inositol trisphosphate (IP3) from the stimulated cell. The two-dimensional model agrees well with experimental data and makes the following quantitative predictions: as the distance from the stimulated cells increases, 1) the intercellular delay increases exponentially, 2) the intracellular wave speed decreases exponentially, and 3) the arrival time increases exponentially. Furthermore, 4) a proportion of the cells at the periphery of the response will exhibit waves of decreased amplitude, 5) the intercellular membrane permeability to IP3 must be approximately 2 microns/s or greater, and 6) the ratio of the maximum concentration of IP3 in the stimulated cell to the Km of the IP3 receptor (with respect to IP3) must be approximately 300 or greater. These predictions constitute a rigorous test of the hypothesis that the intercellular Ca2+ waves are mediated by IP3 diffusion.
48
McCarron, John G., Susan Chalmers, Debbi MacMillan, and Marnie L. Olson. "Agonist-Evoked Calcium Wave Progression Requires Calcium and Ip3 in Smooth Muscle." Biophysical Journal 98, no. 3 (January 2010): 293a—294a. http://dx.doi.org/10.1016/j.bpj.2009.12.1599.
Full text
49
Prajer, M., A. Fleury, and M. Laurent. "Dynamics of calcium regulation in Paramecium and possible morphogenetic implication." Journal of Cell Science 110, no. 5 (March 1, 1997): 529–35. http://dx.doi.org/10.1242/jcs.110.5.529.
Full textAbstract:
This paper is the first report of the use of a fluorescent indicator (Dextran-coupled calcium green-1) for imaging of cytosolic free calcium in ciliate cells. Using this technique in Paramecium, we show that a very transient increase in the mean intracellular calcium concentration accompanied exocytosis. It has long been postulated based on indirect experimental evidence, that a calcium wave which would spread across the cortex at the time of cell division, would be the primary event that triggers morphogenesis in these species. We theoretically show that a unifying interpretation can be given for the possible occurrence of a single wave and that of multiple oscillations of cytosolic calcium: both of which correspond to two different behaviors of the same dynamic system. Experimental conditions allowing the visualization of possible calcium periodicities in the interphase Paramecium cell are much more easily fulfilled than those permitting the observation of a single wave at the time of cell division. Hence, experiments were performed on interphase cells. After microinjection of calcium indicator into a mutant strain which is defective in exocytosis, we observed Ca2+ oscillations with a period close to 2 minutes. Hence, we conclude that Paramecium possesses all the dynamic elements required to generate, at the time of cell division, a morphogenetic calcium wave.
50
Matese, John C., and David R. McClay. "Cortical granule exocytosis is triggered by different thresholds of calcium during fertilisation in sea urchin eggs." Zygote 6, no. 1 (February 1998): 55–63. http://dx.doi.org/10.1017/s0967199400005086.
Full textAbstract:
SummaryIn sea urchin eggs, fertilisation is followed by a calcium wave, cortical granule exocytosis and fertilisation envelope elevation. Both the calcium wave and cortical granule exocytosis sweep across the egg in a wave initiated at the point of sperm entry. Using differential interference contrast (DIC) microscopy combined with laser scanning confocal microscopy, populations of cortical granules undergoing calcium-induced exocytosis were observed in living urchin eggs. Calcium imaging using the indicator Calcium Green-dextran was combined with an image subtraction technique for visual isolation of individual exocytotic events. Relative fluorescence levels of the calcium indicator during the fertilisation wave were compared with cortical fusion events. In localised regions of the egg, there is a 6s delay between the detection of calcium release and fusion of cortical granules. The rate of calcium accumulation was altered experimentally to ask whether this delay was necessary to achieve a threshold concentration of calcium to trigger fusion, or was a time-dependent activation of the cortical granule fusion apparatus after the ‘triggering’ event. Calcium release rate was attenuated by blocking inositol 1,4,5-triphospate (InsP3)-gated channels with heparin. Heparin extended the time necessary to achieve a minimum concentration of calcium at the sites of cortical granule exocytosis. The data are consistent with the conclusion that much of the delay observed normally is necessary to reach threshold concentration of calcium. Cortical granules then fuse with the plasma membrane. Further, once the minimum threshold calcium concentration is reached, cortical granule fusion with the plasma membrane occurs in a pattern suggesting that cortical granules are non-uniform in their calcium sensitivity threshold.