Mechanisms and function of intercellular calcium signaling

Sanderson, Michael J.; Charles, Andrew; Boitano, Scott; Dirksen, Ellen R.

doi:10.1016/0303-7207(94)90136-8

Cited by 285 publications

(176 citation statements)

References 92 publications

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“…Taken together, it is unlikely that the repetitive Ca2+ spikes observed in the present study can be explained by intercellular diffusion of second messengers or a per iodic release of Ca2+ from intracellular stores as has been proposed in other cell types [2,23,36], Instead, this high degree of synchronisation suggests a rapidly propagating, regenerative electrical signal, i.e. an action potential.…”

Section: Ca2+ Spikingsupporting

confidence: 56%

“…In most cases, the underlying mechanism was unknown. In other cell types, intercellularly propagating Ca2+ waves have been reported [30,33,34] that probably result from the regenerative production of IP3 by the diffusion of Ca2+ and/or IP3 through gap junctions to neighbouring cells with concomitant Ca2+ release from intracellular stores [2].…”

Section: Discussion Synchronised Ca2+ Spiking Of Density-arrested Nrkmentioning

confidence: 99%

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Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

et al. 1997

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SummaryThe correlation between the intracellular Ca2+ concentration ([Ca2+].) and membrane potential in monolayers of density-arrested normal rat kidney (NRK) fibroblasts was investigated. Using the fluorescent probe Fura-2, spontaneous repetitive spike-like increases in [Ca2+]. (Ca2+ spikes) were observed that were synchronised throughout the entire monolayer. Ca2+ spikes disappeared in Ca2+-free solutions and could be blocked by the L-type Ca2* channel antagonist felodipine. Simultaneous measurements of [Ca2+], and membrane potential showed that these Ca2+ spikes were paralleled by depolarisations of the plasma membrane. Using patch clamp measurements, action potential-like depolarisations consisting of a fast spike depolarisation followed by a plateau phase were seen with similar kinetics as the Ca2+ spikes. The action potentials could be blocked by L-type Ca2+ channel blockers and were dependent on extracellular Ca2+. The plateau phase was predominantly determined by a Cl-conductance and was dependent on intracellular Ca2+. The presence of voltage-dependent L-type Ca2+ channels in NRK cells was confirmed by patch clamp measurements in single cells. It is concluded that monolayers of density-arrested NRK fibroblasts exhibit spontaneous Ca2+ action potentials leading to synchronised Ca2+ spiking. This excitability of monolayers of fibroblasts may represent a novel Ca2+ signaling pathway in electrically coupled fibroblasts, cells that were hitherto considered to be inexcitable.

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Section: Ca2+ Spikingsupporting

confidence: 56%

Section: Discussion Synchronised Ca2+ Spiking Of Density-arrested Nrkmentioning

confidence: 99%

Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

et al. 1997

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“…The slower calcium signals in nonexcitable cells typically rely on IP 3 , which binds to channels (InsP 3-Rs) on the endoplasmic reticulum, or potentially nicotinic acid adenine dinucleotide phosphate-gated calcium channels (two pore channels) on acidic organelles, leading to release of calcium into the cytoplasm (Galione 2011). Calcium signals can also pass through gap junctions to coordinate activities of neighboring cells (Sanderson et al 1994).…”

Section: MD Bootmanmentioning

confidence: 99%

Calcium Signaling

Bootman

2012

Cold Spring Harbor Perspectives in Biology

130

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“…I n response to an increased concentration of inositol trisphosphate (IP 3 ), oscillations in the concentration of free intracellular calcium (Ca 2ϩ ) occur in many cell types and are important for the control of many cellular functions (1)(2)(3)(4). In nonexcitable cells, such as epithelial cells, these oscillations occur as the result of Ca 2ϩ flux into and out of the endoplasmic reticulum (ER).…”

mentioning

confidence: 99%

Control of calcium oscillations by membrane fluxes

Sneyd

Tsaneva-Atanasova

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

125

116

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It is known that Ca 2؉ influx plays an important role in the modulation of inositol trisphosphate-generated Ca 2؉ oscillations, but controversy over the mechanisms underlying these effects exists. In addition, the effects of blocking membrane transport or reducing Ca 2؉ entry vary from one cell type to another; in some cell types oscillations persist in the absence of Ca 2؉ entry (although their frequency is affected), whereas in other cell types oscillations depend on Ca 2؉ entry. We present theoretical and experimental evidence that membrane transport can control oscillations by controlling the total amount of Ca 2؉ in the cell (the Ca 2؉ load). Our model predicts that the cell can be balanced at a point where small changes in the Ca 2؉ load can move the cell into or out of oscillatory regions, resulting in the appearance or disappearance of oscillations. Our theoretical predictions are verified by experimental results from HEK293 cells. We predict that the role of Ca 2؉ influx during an oscillation is to replenish the Ca 2؉ load of the cell. Despite this prediction, even during the peak of an oscillation the cell or the endoplasmic reticulum may not be measurably depleted of Ca 2؉ .I n response to an increased concentration of inositol trisphosphate (IP 3 ), oscillations in the concentration of free intracellular calcium (Ca 2ϩ ) occur in many cell types and are important for the control of many cellular functions (1-4). In nonexcitable cells, such as epithelial cells, these oscillations occur as the result of Ca 2ϩ flux into and out of the endoplasmic reticulum (ER). However, although the oscillations result from the cycling of Ca 2ϩ between the ER and the cytoplasm, the transport of Ca 2ϩ across the cell membrane can have a dramatic effect on these oscillations.Although Ca 2ϩ influx is known to be important, disagreement exists, first, over the mechanisms by which Ca 2ϩ influx is modulated during a Ca 2ϩ oscillation, and, second, over the role played by Ca 2ϩ influx. The capacitative entry hypothesis proposes that depletion of ER Ca 2ϩ causes enhanced entry of Ca 2ϩ across the plasma membrane (5-9). Often, although not necessarily, in this scenario, Ca 2ϩ entry is necessary for the refilling of the ER, and thus oscillation frequency is controlled by the refilling time (10, 11). Although capacitative entry is certainly an important factor during the response to a maximal stimulus, other investigators have pointed to a lack of direct evidence that it plays an important role during smaller stimuli that generate oscillatory behavior (12). They maintain that Ca 2ϩ influx, under these conditions, is controlled by a noncapacitative pathway involving arachidonic acid and that the purpose of the influx is to increase the likelihood that low levels of IP 3 will induce Ca 2ϩ release from internal stores (13). This controversy is complicated by the fact that, in some cell types, Ca 2ϩ oscillations persist in the absence of Ca 2ϩ influx (14-16), whereas in other cell types, oscillations depend absolutely on influx (17, ...

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Mechanisms and function of intercellular calcium signaling

Cited by 285 publications

References 92 publications

Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

Calcium Signaling

Control of calcium oscillations by membrane fluxes

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