Synchronous calcium oscillations and calcium waves induced by spatiotemporal noise in a randomly coupled ensemble of neurons

Calcium oscillations occur during meiotic maturation of mouse oocytes. They also trigger activation at fertilization. We have monitored [Ca2+]i in oocytes at different stages of growth and maturation to examine how the calcium release mechanisms alter during oogenesis. Spontaneous calcium oscillations occur every 2–3 minutes in the majority of fully grown (but immature) mouse oocytes released from antral follicles and resuming meiosis. The oscillations last for 2–4 hours after release from the follicle and take the form of global synchronous [Ca2+]i increases throughout the cell. Rapid image acquisition or cooling the bath temperature from 28 degrees C to 16 degrees C did not reveal any wave-like spatial heterogeneity in the [Ca2+]i signal. Calcium appears to reach highest levels in the germinal vesicle but this apparent difference of [Ca2+] in nucleus and cytoplasm is an artifact of dye loading. Smaller, growing immature oocytes are less competent: about 40% are able to resume meiosis and a similar proportion of these oocytes show spontaneous calcium oscillations. [Ca2+]i transients are not seen in oocytes that do not resume meiosis spontaneously in vitro. Nonetheless, these oocytes are capable of [Ca2+]i oscillations since they show them in response to the addition of carbachol or thimerosal. To examine how the properties of calcium release change during meiotic maturation, a calcium-releasing factor from sperm was microinjected into fully grown immature and mature oocytes. The sperm-factor-induced oscillations were about two-fold larger and longer in mature oocytes compared to immature oocytes. Calcium waves travelling at 40–60 microns/second were generated in mature oocytes, but not in immature oocytes. In some mature oocytes, successive calcium waves had different sites of origin. The modifications in the size and spatial organization of calcium transients during oocyte maturation may be a necessary prerequisite for normal fertilization.

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Calcium oscillations and calcium waves coordinate rhythmic contractile activity within the stellate cell layer of medaka fish embryos

Journal of Experimental Zoology ◽

10.1002/jez.1402730205 ◽

1995 ◽

Vol 273 (2) ◽

pp. 118-129 ◽

Cited By ~ 13

Author(s):

Joanne Z. Simon ◽

Mark S. Cooper

Keyword(s):

Cell Layer ◽

Stellate Cell ◽

Contractile Activity ◽

Calcium Oscillations ◽

Calcium Waves ◽

Medaka Fish ◽

Fish Embryos ◽

Rhythmic Contractile Activity

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Ca2+ oscillations, waves, and networks in islets from human donors with and without type 2 diabetes

10.1101/2021.12.08.471749 ◽

2021 ◽

Author(s):

Marko Gosak ◽

Richard Yan-Do ◽

Haopeng Lin ◽

Patrick E Macdonald ◽

Andraz Stozer

Keyword(s):

Type 2 Diabetes ◽

Calcium Imaging ◽

Large Fraction ◽

Human Islets ◽

Calcium Oscillations ◽

Calcium Waves ◽

Intercellular Coupling ◽

Reduced Activity ◽

Glucose Dependence

Pancreatic islets are highly interconnected structures that produce pulses of insulin and other hormones, maintaining normal homeostasis of glucose and other nutrients. Normal stimulus-secretion and intercellular coupling are essential to regulated secretory responses and these hallmarks are known to be altered in diabetes. In the present study, we used calcium imaging of isolated human islets to assess their collective cell behavior. The activity occurred in the form of calcium oscillations, was synchronized across different regions of islets through calcium waves, and was glucose-dependent: higher glucose enhanced the activity, elicited a greater proportion of global calcium waves, and led to denser and less fragmented functional networks. Hub regions were identified in stimulatory conditions, and they represented the most active islet regions. Moreover, calcium waves were found to be initiated in different subregions and the roles of initiators and hubs did not overlap. In type 2 diabetes, glucose-dependence was retained, but a reduced activity, locally restricted waves, and more segregated networks were detected compared with control islets. Interestingly, hub regions seemed to suffer the most by losing a disproportionately large fraction of connections. These changes affected islets from donors with diabetes in a heterogeneous manner.

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Activation of a cGMP-sensitive calcium-dependent chloride channel may cause transition from calcium waves to whole cell oscillations in smooth muscle cells

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00726.2006 ◽

2007 ◽

Vol 293 (1) ◽

pp. H215-H228 ◽

Cited By ~ 24

Author(s):

Jens Christian Brings Jacobsen ◽

Christian Aalkjær ◽

Holger Nilsson ◽

Vladimir V. Matchkov ◽

Jacob Freiberg ◽

...

Keyword(s):

Smooth Muscle ◽

Membrane Potential ◽

Smooth Muscle Cells ◽

Chloride Channel ◽

Muscle Cells ◽

Calcium Oscillations ◽

Calcium Waves ◽

Whole Cell ◽

Calcium Dependent ◽

The Individual

In vitro, α-adrenoreceptor stimulation of rat mesenteric small arteries often leads to a rhythmic change in wall tension, i.e., vasomotion. Within the individual smooth muscle cells of the vascular wall, vasomotion is often preceded by a period of asynchronous calcium waves. Abruptly, these low-frequency waves may transform into high-frequency whole cell calcium oscillations. Simultaneously, multiple cells synchronize, leading to rhythmic generation of tension. We present a mathematical model of vascular smooth muscle cells that aims at characterizing this sudden transition. Simulations show calcium waves sweeping through the cytoplasm when the sarcoplasmic reticulum (SR) is stimulated to release calcium. A rise in cGMP leads to the experimentally observed transition from waves to whole cell calcium oscillations. At the same time, membrane potential starts to oscillate and the frequency approximately doubles. In this transition, the simulated results point to a key role for a recently discovered cGMP-sensitive calcium-dependent chloride channel. This channel depolarizes the membrane in response to calcium released from the SR. In turn, depolarization causes a uniform opening of L-type calcium channels on the cell surface, stimulating a synchronized release of SR calcium and inducing the shift from waves to whole cell oscillations. The effect of the channel is therefore to couple the processes of the SR with those of the membrane. We hypothesize that the shift in oscillatory mode and the associated onset of oscillations in membrane potential within the individual cell may underlie sudden intercellular synchronization and the appearance of vasomotion.

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