Sperm and Its Soluble Extract Cause Transient Increases in Intracellular Calcium Concentration and in Membrane Potential of Sea Urchin Zygotes

1994 ◽  
Vol 166 (1) ◽  
pp. 268-276 ◽  
Author(s):  
Masaki Osawa ◽  
Kazuhisa Takemoto ◽  
Munehiro Kikuyama ◽  
Hiroyuki Uchiyama ◽  
Yukio Hiramoto ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Sea Urchin ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Soluble Extract

Lighting the fuse at fertilization

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 1-12 ◽  
Author(s):  
M. Whitaker ◽  
K. Swann
Keyword(s):  
Signal Transduction ◽  
Plasma Membrane ◽  
Intracellular Calcium ◽  
G Protein ◽  
Sea Urchin ◽  
Calcium Concentration ◽  
Cell Signalling ◽  
Somatic Cells ◽  
Intracellular Calcium Concentration ◽  
Transmembrane Signalling

In most deuterostome eggs, fertilization is marked by an abrupt and transient increase in intracellular calcium concentration. The transient takes the form of a propagating wave and is the signal for the onset of development. For those interested in cell signalling, the two obvious questions to ask are how the wave is initiated and how it propagates through the egg cytoplasm. Answers have come largely from experiments in frog, hamster, mouse and sea urchin eggs. One explanation of signal transduction at fertilization makes an analogy with transmembrane signalling in somatic cells, where a family of G-protein-linked receptors pass activating signals across the plasma membrane. Another, older idea is that it is the fusion of sperm and egg that is responsible for detonating the calcium explosion at fertilization. We discuss the relative merits of the two ideas. Both are plausible; the creative tension between them has led to experiments that broaden our view of signal transduction at fertilization.

Changes in Membrane Potential and the Intracellular Calcium Concentration During CSD and OGD in Layer V and Layer II/III Mouse Cortical Neurons

2010 ◽  
Vol 104 (6) ◽  
pp. 3203-3212 ◽  
Author(s):  
Helen M. Gniel ◽  
Rosemary L. Martin
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Cortical Neurons ◽  
Calcium Concentration ◽  
Pyramidal Neurons ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Intracellular Calcium Concentration ◽  
Neuronal Types ◽  
Layer V

Cortical spreading depression (CSD) is an episode of electrical silence following intense neuronal activity that propagates across the cortex at ∼3–6 mm/min and is associated with transient neuronal depolarization. CSD is benign in normally perfused brain tissue, but there is evidence suggesting that repetitive CSD contributes to infarct growth following focal ischemia. Studies to date have assumed that the cellular responses to CSD are uniform across neuronal types because there are no data to the contrary. In this study, we investigated the effect of CSD on membrane potential and the intracellular calcium concentration ([Ca2+]i) of mouse layer V and layer II/III pyramidal neurons in brain slices. To place the data in context, we made similar measurements during anoxic depolarization induced by oxygen and glucose deprivation (OGD). The [Ca2+]i was quantified using the low-affinity ratiometric indicator Fura-4F. During both CSD- and OGD-induced depolarization, the membrane potential approached 0 mV in all neurons. In layer V pyramids OGD resulted in an increase in [Ca2+]i to a maximum of 3.69 ± 0.73 (SD) μM ( n = 12), significantly greater than the increase to 1.81 ± 0.70 μM in CSD ( n = 34; P < 0.0001). Membrane potential and [Ca2+]i returned to nearly basal levels following CSD but not OGD. Layer II/III neurons responded to CSD with a greater peak increase in [Ca2+]i than layer V neurons (2.88 ± 0.6 μM; n = 9; P < 0.01). We conclude there is a laminar difference in the response of pyramidal neurons to CSD; possible explanations are discussed.

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