scholarly journals Membrane potential change in a sea urchin egg induced by calcium ionophore A23187 has the same component that is involved in the fertilization potential.

1989 ◽  
Vol 14 (6) ◽  
pp. 697-706
Author(s):  
Shuichi Obata ◽  
Hideyo Kuroda
Keyword(s):  
Membrane Potential ◽  
Sea Urchin ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Potential Change ◽  
Ionophore A23187 ◽  
Membrane Potential Change ◽  
Sea Urchin Egg

scholarly journals Interrelationships of polymorphonuclear neutrophil membrane-bound calcium, membrane potential, and chemiluminescence: studies in single living cells

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1184-1192 ◽  
Author(s):  
GW Sullivan ◽  
GR Donowitz ◽  
JA Sullivan ◽  
GL Mandell
Keyword(s):  
Membrane Potential ◽  
Calcium Release ◽  
Calcium Ionophore ◽  
Image Intensifier ◽  
Calcium Ionophore A23187 ◽  
Polymorphonuclear Neutrophil ◽  
Human Neutrophils ◽  
Ionophore A23187 ◽  
Ionic Fluxes ◽  
Single Living

Abstract Stimulated neutrophils show ionic fluxes that may function as “transducers” between stimuli and effector functions. Using fluorescent probes, patterns of membrane-associated calcium (chlortetracycline, CTC) and membrane potential (3–3′-dipentyloxacarbocyanine, di-O-C5 (3)) in single living human neutrophils were observed with a fluorescence microscope fitted with an image intensifier and photometer. Fluorescence changes were related to chemiluminescence. In unstimulated neutrophils, CTC and di-O-C5 (3) fluorescence was brightest in the perinuclear region. Di-O-C5 (3) fluorescence was also seen in mitochondria. Neutrophil stimulation with zymosan, phorbol myristate acetate (PMA) or calcium ionophore (A23187) resulted in loss of di-O-C5 (3) and CTC fluorescence and chemiluminescence proportional to the strength of the stimulus. Experiments demonstrated the independence of these processes. (1) Digitonin stimulation caused chemiluminescence and di-O-C5 (3) darkening without loss of CTC fluorescence. (2) Depolarization of neutrophils did not induce CTC darkening or chemiluminescence. (3) Calcium ionophore (A23187) stimulation of neutrophils in calcium-free medium resulted in normal di-O-C5 (3) and CTC darkening, but a blunted chemiluminescence peak. (4) Calcium ionophore (A23187) stimulated the loss of di-O-C5 (3) and CTC fluorescence from chronic granulomatous disease neutrophils, but did not trigger an oxidative burst. Although neutrophil depolarization, calcium release from membranes, and oxidative activity are linked, these processes can clearly be separated.

scholarly journals Structural organization of actin in the sea urchin egg cortex: microvillar elongation in the absence of actin filament bundle formation

1982 ◽  
Vol 93 (1) ◽  
pp. 24-32 ◽  
Author(s):  
DA Begg ◽  
LI Rebhun ◽  
H Hyatt
Keyword(s):  
Sea Urchin ◽  
Actin Filament ◽  
Actin Filaments ◽  
Calcium Ionophore ◽  
Ionophore A23187 ◽  
Acid Activation ◽  
Cytoplasmic Ph ◽  
Sea Urchin Egg ◽  
Filament Bundles ◽  
Filament Bundle

We have investigated the relationship between the formation of actin filament bundles and the elongation of microvilli (MV) after fertilization in sea urchin eggs. In a previous study (1979, J Cell Biol. 83:241-248) we demonstrated that increased pH induced the formation of actin filaments in isolated sea urchin egg cortices with the concomitant elongation of MV. On the basis of these results we suggested that increased cytoplasmic pH after fertilization causes a reorganization of cortical actin, which in turn provides the force for MV elongation. To test this hypothesis, we compared the morphology of microvilli in eggs activated with and without the release of fertilization acid. Activation of eggs in normal sea water with the calcium ionophore A23187 causes the release of fertilization acid and the elongation of MV containing core bundles of actin filaments. Eggs activated with A23187 in NA(+)-free water do not undergo normal fertilization acid release but develop elongated, flaccid MV. These MV contain an irregular network of actin filaments rather than the parallel bundles of filaments found in normal MV. The addition of 40 mM NaCl to these eggs results in the release of H(+) and the concomitant conversion of flaccid MV to erect MV containing typical core bundles of actin filaments. Identical results are obtained when 10 mM NH(4)Cl is substituted for NaCl. The induction of cytoplasmic alkalinization in unactivated eggs with NH(4)Cl does not cause either MV elongation or the formation of actin filament bundles . These results suggest that: (a) the elongation of MV is stimulated by a rise in intracellular free Ca(++) concentration; (b) actin filament bundle formation is triggered by an increase in cytoplasmic pH; and (c) the formation of actin filament bundles is not necessary for MV elongation but is required to provide rigid support for MV.

scholarly journals Early plasma-membrane-potential changes during stimulation of lymphocytes by concanavalin A.

1983 ◽  
Vol 210 (3) ◽  
pp. 885-891 ◽  
Author(s):  
S M Felber ◽  
M D Brand
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Concanavalin A ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
K Channel ◽  
Ionophore A23187 ◽  
Resting Cells ◽  
Plasma Membrane Potential ◽  
Stimulation Of

1. We have monitored the plasma-membrane potential of lymphocytes by measuring the accumulation of the lipophilic cation methyltriphenylphosphonium (TPMP+) in the presence of the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP). 2. The mitogen concanavalin A causes a decrease in TPMP+ accumulation by pig lymphocytes corresponding to a 3 mV depolarization with 2 1/2 min. Concanavalin A does not alter 86Rb+ uptake in the first 30 min. 3. In contrast concanavalin A increased TPMP+ accumulation and the rate of Rb+ uptake in mouse thymocytes. This is consistent with a previous proposal that the mitogen induces a hyperpolarization of mouse thymocytes as a result of stimulation of a Ca2+-dependent K+ channel. 4. Studies with the calcium ionophore A23187 and quinine (an inhibitor of the Ca2+-dependent K+ channel) suggest that the channel is partially closed in mouse resting thymocytes but is almost fully active in pig resting cells. Thus concanavalin A hyperpolarizes mouse thymocytes by activating the Ca2+-dependent K+ channel but cannot do so in pig lymphocytes because the channel is already maximally activated. 5. The 3mV depolarization of pig cells cannot be explained by a decrease in electrogenic K+ permeability.

scholarly journals Interrelationships of polymorphonuclear neutrophil membrane-bound calcium, membrane potential, and chemiluminescence: studies in single living cells

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1184-1192
Author(s):  
GW Sullivan ◽  
GR Donowitz ◽  
JA Sullivan ◽  
GL Mandell
Keyword(s):  
Membrane Potential ◽  
Calcium Release ◽  
Calcium Ionophore ◽  
Image Intensifier ◽  
Calcium Ionophore A23187 ◽  
Polymorphonuclear Neutrophil ◽  
Human Neutrophils ◽  
Ionophore A23187 ◽  
Ionic Fluxes ◽  
Single Living

Stimulated neutrophils show ionic fluxes that may function as “transducers” between stimuli and effector functions. Using fluorescent probes, patterns of membrane-associated calcium (chlortetracycline, CTC) and membrane potential (3–3′-dipentyloxacarbocyanine, di-O-C5 (3)) in single living human neutrophils were observed with a fluorescence microscope fitted with an image intensifier and photometer. Fluorescence changes were related to chemiluminescence. In unstimulated neutrophils, CTC and di-O-C5 (3) fluorescence was brightest in the perinuclear region. Di-O-C5 (3) fluorescence was also seen in mitochondria. Neutrophil stimulation with zymosan, phorbol myristate acetate (PMA) or calcium ionophore (A23187) resulted in loss of di-O-C5 (3) and CTC fluorescence and chemiluminescence proportional to the strength of the stimulus. Experiments demonstrated the independence of these processes. (1) Digitonin stimulation caused chemiluminescence and di-O-C5 (3) darkening without loss of CTC fluorescence. (2) Depolarization of neutrophils did not induce CTC darkening or chemiluminescence. (3) Calcium ionophore (A23187) stimulation of neutrophils in calcium-free medium resulted in normal di-O-C5 (3) and CTC darkening, but a blunted chemiluminescence peak. (4) Calcium ionophore (A23187) stimulated the loss of di-O-C5 (3) and CTC fluorescence from chronic granulomatous disease neutrophils, but did not trigger an oxidative burst. Although neutrophil depolarization, calcium release from membranes, and oxidative activity are linked, these processes can clearly be separated.

Induction of shape transformation in sea urchin coelomocytes by the calcium ionophore A23187

Cell Motility ◽  
1984 ◽  
Vol 4 (1) ◽  
pp. 57-71 ◽  
Author(s):  
Hilary A. Hyatt ◽  
Michael S. Shure ◽  
David A. Begg
Keyword(s):  
Sea Urchin ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Shape Transformation

Intracellular pH increase accompanies parthenogenetic activation of porcine, bovine and murine oocytes

2000 ◽  
Vol 12 (4) ◽  
pp. 201 ◽  
Author(s):  
Nancy T. Ruddock ◽  
Zoltán Macháty ◽  
Randall S. Prather
Keyword(s):  
Intracellular Ph ◽  
Prolonged Exposure ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Oocyte Activation ◽  
Parthenogenetic Activation ◽  
Sea Urchin Egg ◽  
Porcine Oocyte ◽  
Bovine Oocytes

Although an intracellular pH (pH i ) increase at the time of fertilization is necessary for activation of the sea urchin egg, recent reports in the mouse and rat have indicated that there is not a pHi increase during fertilization or during 7% ethanol activation in the mouse. It has been suggested that mammals may have lost the need for a pH i increase at the time of fertilization and the present study reports significant pH i changes during parthenogenetic activation of porcine IVM oocytes, as well as pH i responses to activation in bovine and murine oocytes. Transient intracellular pH changes were found during porcine oocyte activation when using 7% ethanol and with 50 or 100 M calcium ionophore (A23187). Treatment with 200 M thimerosal resulted in an increase in pH i after a delay of approximately 12 min. Murine oocytes showed a significant increase during activation with 7% ethanol and A23187 as well as during prolonged exposure to thimerosal. Bovine oocytes exhibited an increase in pH i only when activated with 50 or 100 M A23187. The final set of experiments aimed to determine whether the porcine oocyte has mechanisms to alleviate induced acidic and alkaline challenges. Both acidic (~20 mM acetic acid) and alkaline (~30 mM ammonium chloride) challenges caused significant changes in pH i that porcine IVM oocytes were capable of recovering from within 35 min. Future studies will focus on determining which of the mechanisms is producing the pH i increase at the time of parthenogenetic activation in the porcine oocyte.

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)

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