Soluble extracts from ascidian spermatozoa trigger intracellular calcium release independently of the activation of the ADP ribose channel

We have injected soluble extracts of sperm from the ascidian Ciona intestinalis into oocytes of the same species to test whether these extracts can mimic the events of fertilisation. Injection of ascidian sperm extracts leads, after a delay of approximately 60 s, to a large calcium transient and repetitive pattern of calcium oscillations, mimicking the normal fertilisation response. The response was concentration-independent, suggesting a stimulatory mechanism in triggering the fertilisation response. We tested the pathway of calcium release in ascidian oocytes after injection of sperm extracts by preinjection of calcium release inhibitors. The data demonstrate that dual pathways to calcium release act at fertilisation in ascidians, as in other species. C. intestinalis oocytes are characterised by a nion channel in the plasma membrane that is gated uniquely by ADP ribose. We show that this channel is not gated by the injection of ascidian sperm extracts. Our data suggest that one metabolic pathway triggered by sperm, the release of nitric oxide, is not stimulated by sperm extracts and that several metabolic pathways are stimulated at fertilisation by more than one factor within sperm.

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Caffeine attenuates contraction-induced diminutions of the intracellular calcium transient in mouse lumbrical muscle ex vivo

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2018-0658 ◽

2019 ◽

Vol 97 (5) ◽

pp. 429-435 ◽

Cited By ~ 2

Author(s):

Ian C. Smith ◽

Rene Vandenboom ◽

A. Russell Tupling

Keyword(s):

Skeletal Muscle ◽

Intracellular Calcium ◽

Calcium Release ◽

Ex Vivo ◽

Calcium Transient ◽

Calcium Transients ◽

Inotropic Effects ◽

Intracellular Calcium Transient ◽

Lumbrical Muscle ◽

Lumbrical Muscles

The amount of calcium released from the sarcoplasmic reticulum in skeletal muscle rapidly declines during repeated twitch contractions. In this study, we test the hypothesis that caffeine can mitigate these contraction-induced declines in calcium release. Lumbrical muscles were isolated from male C57BL/6 mice and loaded with the calcium-sensitive indicator, AM-furaptra. Muscles were then stimulated at 8 Hz for 2.0 s in the presence or absence of 0.5 mM caffeine, at either 30 °C or 37 °C. The amplitude and area of the furaptra-based intracellular calcium transients and force produced during twitch contractions were calculated. For each of these measures, the values for twitch 16 relative to twitch 1 were higher in the presence of caffeine than in the absence of caffeine at both temperatures. We conclude that caffeine can attenuate contraction-induced diminutions of calcium release during repeated twitch contractions, thereby contributing to the inotropic effects of caffeine.

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Stabilizing Role of Calcium Store-Dependent Plasma Membrane Calcium Channels in Action-Potential Firing and Intracellular Calcium Oscillations

Biophysical Journal ◽

10.1529/biophysj.105.062984 ◽

2005 ◽

Vol 89 (6) ◽

pp. 3741-3756 ◽

Cited By ~ 17

Author(s):

J.M.A.M. Kusters ◽

M.M. Dernison ◽

W.P.M. van Meerwijk ◽

D.L. Ypey ◽

A.P.R. Theuvenet ◽

...

Keyword(s):

Plasma Membrane ◽

Calcium Channels ◽

Action Potential ◽

Intracellular Calcium ◽

Calcium Oscillations ◽

Action Potential Firing ◽

Calcium Store ◽

Potential Firing

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Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

AJP Cell Physiology ◽

10.1152/ajpcell.00046.2011 ◽

2011 ◽

Vol 301 (3) ◽

pp. C679-C686 ◽

Cited By ~ 21

Author(s):

Peter Sobolewski ◽

Judith Kandel ◽

Alexandra L. Klinger ◽

David M. Eckmann

Keyword(s):

Endothelial Cells ◽

Intracellular Calcium ◽

Calcium Release ◽

Transient Receptor Potential ◽

Calcium Influx ◽

Calcium Transient ◽

Epifluorescence Microscopy ◽

Transient Receptor Potential Vanilloid ◽

Calcium Stores ◽

Air Bubble

Gas embolism is a serious complication of decompression events and clinical procedures, but the mechanism of resulting injury remains unclear. Previous work has demonstrated that contact between air microbubbles and endothelial cells causes a rapid intracellular calcium transient and can lead to cell death. Here we examined the mechanism responsible for the calcium rise. Single air microbubbles (50–150 μm), trapped at the tip of a micropipette, were micromanipulated into contact with individual human umbilical vein endothelial cells (HUVECs) loaded with Fluo-4 (a fluorescent calcium indicator). Changes in intracellular calcium were then recorded via epifluorescence microscopy. First, we confirmed that HUVECs rapidly respond to air bubble contact with a calcium transient. Next, we examined the involvement of extracellular calcium influx by conducting experiments in low calcium buffer, which markedly attenuated the response, or by pretreating cells with stretch-activated channel blockers (gadolinium chloride or ruthenium red), which abolished the response. Finally, we tested the role of intracellular calcium release by pretreating cells with an inositol 1,4,5-trisphosphate (IP3) receptor blocker (xestospongin C) or phospholipase C inhibitor (neomycin sulfate), which eliminated the response in 64% and 67% of cases, respectively. Collectively, our results lead us to conclude that air bubble contact with endothelial cells causes an influx of calcium through a stretch-activated channel, such as a transient receptor potential vanilloid family member, triggering the release of calcium from intracellular stores via the IP3 pathway.

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Membrane junctions in xenopus eggs: their distribution suggests a role in calcium regulation

The Journal of Cell Biology ◽

10.1083/jcb.96.4.1159 ◽

1983 ◽

Vol 96 (4) ◽

pp. 1159-1163 ◽

Cited By ~ 92

Author(s):

DM Gardiner ◽

RD Grey

Keyword(s):

Endoplasmic Reticulum ◽

Plasma Membrane ◽

Intracellular Calcium ◽

Calcium Release ◽

Egg Activation ◽

Electron Dense Material ◽

Intracellular Calcium Release ◽

Cortical Endoplasmic Reticulum ◽

Center Distance ◽

Lines Of Evidence

We have observed the presence of membrane junctions formed between the plasma membrane and cortical endoplasmic reticulum of mature, unactivated eggs of xenopus laevis. The parallel, paired membranes of the junction are separated by a 10-mn gap within which electron-dense material is present. This material occurs in patches with an average center-to-center distance of approximately 30 nm. These junctions are rare in immature (but fully grown) oocytes (approximately 2 percent of the plasma membrane is associated with junctions) and increase dramatically during progesterone-induced maturation. Junctions in the mature, unactivated egg are two to three times more abundant in the animal hemisphere (25-30 percent of the plasma membrane associated with junction) as compared with the vegetal hemisphere (10-15 percent). Junction density decreases rapidly to values characteristic of immature oocytes in response to egg activation. The plasma membrane-ER junctions of xenopus eggs are strikingly similar in structure to membrane junctions in muscle cells thought to be essential in the triggering of intracellular calcium release from the sarcoplasmic reticulum. In addition, the junctions' distinctive, animal-vegetal polarity of distribution, their dramatic appearance during maturation, and their disapperance during activation are correlated with previously documented patterns of calcium-mediated events in anuran eggs. We discuss several lines of evidence supporting the hypothesis that these junctions in xenopus eggs are sites that transduce extracellular events into intracellular calcium release during fertilization and activation of development.

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The Integration of Receptor-Regulated Intracellular Calcium Release and Calcium Entry across the Plasma Membrane

Current Topics in Cellular Regulation ◽

10.1016/b978-0-12-152831-7.50004-4 ◽

1990 ◽

pp. 111-127 ◽

Cited By ~ 13

Author(s):

JAMES W. PUTNEY

Keyword(s):

Plasma Membrane ◽

Intracellular Calcium ◽

Calcium Release ◽

Calcium Entry ◽

Intracellular Calcium Release

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The nitric oxide signaling pathway inhibits intracellular calcium release to prevent neurodevelopmental alcohol toxicity

10.17077/etd.2p9eqf4f ◽

2010 ◽

Author(s):

Dimitrios Elias Kouzoukas

Keyword(s):

Nitric Oxide ◽

Intracellular Calcium ◽

Signaling Pathway ◽

Calcium Release ◽

Nitric Oxide Signaling ◽

Intracellular Calcium Release

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Laser backscatter studies of intracellular Ca2+ oscillations in isolated hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.2.h665 ◽

1989 ◽

Vol 257 (2) ◽

pp. H665-H673 ◽

Cited By ~ 2

Author(s):

M. D. Stern ◽

H. F. Weisman ◽

D. G. Renlund ◽

G. Gerstenblith ◽

O. Hano ◽

...

Keyword(s):

Intracellular Calcium ◽

Calcium Release ◽

Scattered Light ◽

Calcium Oscillations ◽

Extracellular Potassium ◽

Base Line ◽

Measured Intensity ◽

Isolated Hearts ◽

Rat Hearts ◽

Intensity Fluctuations

We measured intensity fluctuations of 633 nm laser light backscattered from the epicardial surface of isolated, perfused rat and rabbit hearts. Scattered light intensity fluctuations (SLIF) were detected from verapamil-arrested rat hearts. The frequency of SLIF was increased by maneuvers that raise intracellular calcium. SLIF were abolished by removal of extracellular calcium with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and by blockade of sarcoplasmic reticulum calcium release by ryanodine. SLIF were not accompanied by any surface electro-cardiogram and were not abolished by 144 mM extracellular potassium. SLIF were absent in rabbit hearts under base-line conditions but could be provoked by calcium loading using zero potassium and ouabain. We conclude that backscatter SLIF monitor the microscopic motion caused by intracellular calcium oscillations in the intact heart. We measured SLIF from rat hearts during 60 min of global ischemia at 30 degrees C, followed by reflow. Ischemia reduced SLIF frequency to zero within 30 min. Reflow caused an overshoot of SLIF frequency to as much as five times control, suggesting that reflow causes major calcium overload of cells that are at least transiently viable.

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Fast calcium wave propagation mediated by electrically conducted excitation and boosted by CICR

AJP Cell Physiology ◽

10.1152/ajpcell.00181.2007 ◽

2008 ◽

Vol 294 (4) ◽

pp. C917-C930 ◽

Cited By ~ 9

Author(s):

J. M. A. M. Kusters ◽

W. P. M. van Meerwijk ◽

D. L. Ypey ◽

A. P. R. Theuvenet ◽

C. C. A. M. Gielen

Keyword(s):

Intracellular Calcium ◽

Chloride Channels ◽

Calcium Release ◽

Rat Kidney ◽

Electrical Coupling ◽

Calcium Oscillations ◽

Calcium Wave ◽

Calcium Oscillation ◽

Pacemaker Cell ◽

Pacemaker Cells

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.

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Nicotinamide alters the calcium release pattern and the degradation of MPF activity after fertilisation in ascidian oocytes

Zygote ◽

10.1017/s0967199499000647 ◽

1999 ◽

Vol 7 (3) ◽

pp. 255-260 ◽

Cited By ~ 3

Author(s):

Martin Wilding ◽

Marcella Marino ◽

Daniela Dale

Keyword(s):

Cell Cycle ◽

Plasma Membrane ◽

Intracellular Calcium ◽

Embryo Development ◽

Calcium Release ◽

Calcium Signalling ◽

Membrane Current ◽

Calcium Induced Calcium Release ◽

Nicotinamide Treatment ◽

Meiosis I

Fertilisation in ascidian oocytes triggers a plasma membrane current, the release of intracellular calcium and the degradation of Maturation Promoting Factor (MPF) activity leading to the completion of meiosis and the initiation of embryo development. We have previously shown that the fertilisation current in ascidians is produced through the metabolism of nicotinamide nucleotide (NN) metabolites to ADP ribose. In this study we have used nicotinamide to test whether NN metabolism plays additional roles in fertilisation in ascidians. Nicotinamide treatment blocked calcium-induced calcium release (CICR) and arrested the cell cycle prior to the completion of meiosis I. Nicotinamide further prevented the abolition of MPF activity after fertilisation. Interestingly, nicotinamide treatment caused ascidian oocytes to form interphase-like pronuclei after fertilisation, despite the high MPF activity. The data demonstrate that NN metabolism is involved in calcium signalling through CICR and further suggest that a NN metabolite acts as a messenger connecting MPF activity to the formation of the meiotic apparatus.

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