scholarly journals Internal calcium release and activation of sea urchin eggs by cGMP are independent of the phosphoinositide signaling pathway.

1992 ◽  
Vol 3 (3) ◽  
pp. 373-383 ◽  
Author(s):  
T Whalley ◽  
A McDougall ◽  
I Crossley ◽  
K Swann ◽  
M Whitaker
Keyword(s):  
Signaling Pathway ◽  
Sea Urchin ◽  
Calcium Release ◽  
Ion Concentration ◽  
Free Calcium ◽  
Calcium Stores ◽  
Phosphoinositide Signaling ◽  
Sea Urchin Eggs ◽  
Calcium Ion Concentration ◽  
Internal Calcium

We show that microinjecting cyclic GMP (cGMP) into unfertilized sea urchin eggs activates them by stimulating a rise in the intracellular free calcium ion concentration ([Ca2+]i). The increase in [Ca2+]i is similar in both magnitude and duration to the transient that activates the egg at fertilization. It is due to mobilization of calcium from intracellular stores but is not prevented by the inositol trisphosphate (InsP3) antagonist heparin. Furthermore, cGMP does not stimulate the eggs Na+/H+ antiport when the [Ca2+]i transient is blocked by the calcium chelator bis-(O-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), suggesting that cGMP does not activate eggs by interacting with the their phosphoinositide signaling pathway. However, the [Ca2+]i increase and activation are prevented in eggs in which the InsP3-sensitive calcium stores have been emptied by the prior microinjection of the InsP3 analogue inositol 1,4,5-trisphosphorothioate. These data indicate that cGMP activates eggs by stimulating the release of calcium from an InsP3-sensitive calcium store via a novel, though unidentified, route independent of the InsP3 receptor.

scholarly journals Injection of inositol trisphosphorothioate into Limulus ventral photoreceptors causes oscillations of free cytosolic calcium.

1991 ◽  
Vol 97 (6) ◽  
pp. 1165-1186 ◽  
Author(s):  
R Payne ◽  
B V Potter
Keyword(s):  
Membrane Potential ◽  
Calcium Release ◽  
Feedback Inhibition ◽  
Initial Response ◽  
Periodic Variation ◽  
Cytosolic Calcium ◽  
Ion Concentration ◽  
Free Calcium ◽  
Calcium Stores ◽  
Calcium Ion Concentration

Limulus ventral photoreceptors contain calcium stores sensitive to release by D-myo-inositol 1,4,5 trisphosphate (InsP3) and a calcium-activated conductance that depolarizes the cell. Mechanisms that terminate the response to InsP3 were investigated using nonmetabolizable DL-myo-inositol 1,4,5 trisphosphorothioate (InsPS3). An injection of 1 mM InsPS3 into a photoreceptor's light-sensitive lobe caused an initial elevation of cytosolic free calcium ion concentration (Cai) and a depolarization lasting only 1-2 s. A period of densensitization followed, during which injections of InsPS3 were ineffective. As sensitivity recovered, oscillations of membrane potential began, continuing for many minutes with a frequency of 0.07-0.3 Hz. The activity of InsPS3 probably results from the D-stereoisomer, since L-InsP3 was much less effective than InsP3. Injections of 1 mM InsP3 caused an initial depolarization and a period of densensitization similar to that caused by 1 mM InsPS3, but no sustained oscillations of membrane potential. The initial response to InsPS3 or InsP3 may therefore be terminated by densensitization, rather than by metabolism. Metabolism of InsP3 may prevent oscillations of membrane potential after sensitivity has recovered. The InsPS3-induced oscillations of membrane potential accompanied oscillations of Cai and were abolished by injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Removal of extracellular calcium reduced the frequency of oscillation but not its amplitude. Under voltage clamp, oscillations of inward current were observed. These results indicate that periodic bursts of calcium release underly the oscillations of membrane potential. After each burst, the sensitivity of the cell to injected InsP3 was greatly reduced, recovering during the interburst interval. The oscillations may, therefore, result in part from a periodic variation in sensitivity to a constant concentration of InsPS3. Prior injection of calcium inhibited depolarization by InsPS3, suggesting that feedback inhibition of InsPS3-induced calcium release by elevated Cai may mediate desensitization between bursts and after injections of InsPS3.

scholarly journals Intracellular calcium release is more efficient than calcium influx in stimulating mitochondrial NAD(P)H formation in adrenal glomerulosa cells

1997 ◽  
Vol 328 (2) ◽  
pp. 525-528 ◽  
Author(s):  
Tibor ROHÁCS ◽  
Kálmán TORY ◽  
András DOBOS ◽  
András SPÄT
Keyword(s):  
Calcium Ion ◽  
Calcium Release ◽  
Calcium Influx ◽  
Biological Significance ◽  
Ion Concentration ◽  
Free Calcium ◽  
Mitochondrial Matrix ◽  
Free Medium ◽  
Glomerulosa Cells ◽  
Calcium Ion Concentration

We compared the effect on mitochondrial NAD(P)H formation of calcium release from intracellular stores with that of calcium influx from the extracellular space. Simultaneous measurements of cytoplasmic free calcium ion concentration and mitochondrial NAD(P)H were performed on fura-PE3-loaded single rat adrenal glomerulosa cells. The effects of equipotent stimuli in terms of the evoked Ca2+ response were compared. Angiotensin II (AII; 1 nM) induced a higher amplitude NAD(P)H response than K+ (5.6-7.6 mM). Vasopressin (1 μM) also induced a greater initial NAD(P)H formation than K+, although the Ca2+ signal evoked by the two agonists had similar amplitude. To examine the effect of Ca2+ release from internal stores we applied AII in Ca2+-free medium. We compared the effect on NAD(P)H formation of Ca2+ release with Ca2+ influx induced by K+, and with capacitative Ca2+ influx induced by AII. NAD(P)H formation in response to Ca2+ release was greater than that induced by Ca2+ influx, irrespective of whether induced by K+ or AII. Our results indicate that Ca2+, presumably released in the vicinity of mitochondria, activates mitochondrial dehydrogenases more efficiently than Ca2+ entering through the plasma membrane. These data confirm the biological significance of previous observations showing that Ca2+ released from inositol 1,4,5-trisphosphate-sensitive internal stores increases mitochondrial matrix [Ca2+] to a greater extent than extracellular Ca2+.

scholarly journals Thimerosal reveals calcium-induced calcium release in unfertilised sea urchin eggs

Zygote ◽  
1993 ◽  
Vol 1 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Alex McDougall ◽  
Isabelle Gillot ◽  
Michael Whitaker
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Transient ◽  
Cell Types ◽  
Egg Activation ◽  
Free Calcium ◽  
Slow Increase ◽  
Sea Urchin Eggs ◽  
Calcium Induced Calcium Release

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.

Polyphosphoinositide metabolism during the fertilization wave in sea urchin eggs

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 187-195 ◽  
Author(s):  
B. Ciapa ◽  
B. Borg ◽  
M. Whitaker
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Calcium Ionophore ◽  
Fold Increase ◽  
Calcium Ionophore A23187 ◽  
Calcium Signal ◽  
Free Calcium ◽  
Ionophore A23187 ◽  
Isotopic Equilibrium ◽  
Sea Urchin Eggs

A transient increase in intracellular free calcium is believed to be the signal responsible for the stimulation of the egg metabolism at fertilization and the resumption of the cell cycle. We have studied how the polyphosphoinositides (PPI) turn over at fertilization in sea urchin eggs, in order to determine the relationship between the metabolism of these lipids and the calcium signal. We compare the patterns of PPI turnover that occur during the first minute following fertilization in eggs in which PPI are labelled to steady state with [3H]inositol or [3H]arachidonate with that in which PPI are labelled for a shorter period with [3H]inositol. When eggs are labelled to apparent isotopic equilibrium with either [3H]inositol or [3H]arachidonate, no early increase in [3H]PtdInsP2 occurs while PtdIns decreases slightly. On the contrary, when not labelled to isotopic equilibrium, all [3H]PPI increase during the first 15 seconds following fertilization. We find that, within seconds, fertilization triggers a 600-fold increase in the turnover of PPI, producing an amount of InsP3 apparently sufficient to trigger calcium release. We suggest that phosphoinositidase C and PtdInsP kinase, responsible respectively for the hydrolysis and synthesis of PtdInsP2, are both stimulated to a comparable degree in the first 30 seconds following fertilization and that net changes in the amount of PtdInsP2 at fertilization are very sensitive to the relative levels of activation of the two enzymes. Activating the eggs with the calcium ionophore A23187 showed that both these enzymes are sensitive to calcium, suggesting that calcium-dependent InsP3 production might play a role in the initiation and/or the propagation of the fertilization calcium wave.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile canalicular contraction in the isolated hepatocyte doublet is related to an increase in cytosolic free calcium ion concentration

2008 ◽  
Vol 8 (3) ◽  
pp. 178-183 ◽  
Author(s):  
Sumio Watanabe ◽  
Masahiro Tomono ◽  
Makoto Takeuchi ◽  
Tsuneo Kitamura ◽  
Miyoko Hirose ◽  
...  
Keyword(s):  
Calcium Ion ◽  
Ion Concentration ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Bile Canalicular Contraction ◽  
Calcium Ion Concentration

scholarly journals The gravistimulation-induced very slow Ca2+ increase in Arabidopsis seedlings requires MCA1, a Ca2+-permeable mechanosensitive channel

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masataka Nakano ◽  
Takuya Furuichi ◽  
Masahiro Sokabe ◽  
Hidetoshi Iida ◽  
Hitoshi Tatsumi
Keyword(s):  
Calcium Ion ◽  
Channel Blocker ◽  
Upright Position ◽  
Ion Concentration ◽  
Early Event ◽  
Free Calcium ◽  
Permeable Channel ◽  
Mechanosensitive Ion Channel ◽  
And Function ◽  
Calcium Ion Concentration

AbstractGravity is a critical environmental factor affecting the morphology and function of plants on Earth. Gravistimulation triggered by changes in the gravity vector induces an increase in the cytoplasmic free calcium ion concentration ([Ca2+]c) as an early process of gravity sensing; however, its role and molecular mechanism are still unclear. When seedlings of Arabidopsis thaliana expressing apoaequorin were rotated from the upright position to the upside-down position, a biphasic [Ca2+]c-increase composed of a fast-transient [Ca2+]c-increase followed by a slow [Ca2+]c-increase was observed. We find here a novel type [Ca2+]c-increase, designated a very slow [Ca2+]c-increase that is observed when the seedlings were rotated back to the upright position from the upside-down position. The very slow [Ca2+]c-increase was strongly attenuated in knockout seedlings defective in MCA1, a mechanosensitive Ca2+-permeable channel (MSCC), and was partially restored in MCA1-complemented seedlings. The mechanosensitive ion channel blocker, gadolinium, blocked the very slow [Ca2+]c-increase. This is the first report suggesting the possible involvement of MCA1 in an early event related to gravity sensing in Arabidopsis seedlings.

Dependence of Cardiac Contractility on Myofibrillar Calcium Sensitivity

Physiology ◽  
1987 ◽  
Vol 2 (5) ◽  
pp. 179-182
Author(s):  
JC Ruegg
Keyword(s):  
Calcium Ion ◽  
Sarcomere Length ◽  
Cardiac Contractility ◽  
Calcium Sensitivity ◽  
Ion Concentration ◽  
Free Calcium ◽  
Wide Range ◽  
Heart Contractility ◽  
Calcium Ion Concentration

In the heart, contractility may be varied over a wide range. It is determined mainly by the myoplasmic free calcium ion concentration. However, alteration of the responsiveness of the myofilaments to calcium may also be important in regulating cardiac contractility, in particular following changes in sarcomere length, or in hypoxia, or after interventions with certain novel cardiotonic drugs.

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