Calcium signalling in non-excitable cells: Notes on oscillations and store refilling

Rink, T J; Hallam, Trevor J.

doi:10.1016/0143-4160(89)90064-x

Cited by 71 publications

(14 citation statements)

References 38 publications

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“…In some non-excitable cells, it has been suggested that the intracellular Ca2+ stores may regulate a pathway for Ca2" entry [5][6][7][8][9]. Evidence for this influx pathway comes from the finding that stores depleted by agonist stimulation in the absence of extracellular Ca2+ may be replenished on exposure to Ca2 , in the absence of agonist, without a rise in [Ca2+]i.…”

Section: Introductionmentioning

confidence: 97%

ADP evokes biphasic Ca2+ influx in fura-2-loaded human platelets. Evidence for Ca2+ entry regulated by the intracellular Ca2+ store

Sage

Reast

Rink³

1990

Biochemical Journal

153

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Stopped-flow fluorimetric studies at 37°C have shown that ADP, at optimal concentrations, can evoke Ca2l or Mn2" influx in fura-2-loaded human platelets without measurable delay. In contrast, the release of Ca2" from intracellular stores is delayed in onset by about 200 ms. By working at a lower temperature, 17°C, we have now shown that the rise in cytosolic calcium concentration ([Ca2+]1) evoked by ADP in the presence of external Ca2" is biphasic. The use of Mn2" as a tracer for bivalent-cation entry indicates that both phases of the ADP-evoked response are associated with influx. The fast phase of the ADP-evoked rise in [Ca2+]i, which occurs without measurable delay at both 17°C and 37°C, is consistent with Ca2" entry mediated by receptor-operated channels in the plasma membrane. The delayed phase, indicated by Mn2" quench, is coincident with the discharge of the intracellular Ca2" stores. Similarly, blockade of the early phase of Ca2' entry by SK&F 96365 further delays the second phase. It is suggested that a pathway for Ca2' entry which is regulated by the intracellular Ca2+ store exists in platelets. This pathway operates alongside, and appears to be modulated by the activity of, other routes for Ca2' entry into the cytosol.

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Section: Introductionmentioning

confidence: 97%

ADP evokes biphasic Ca2+ influx in fura-2-loaded human platelets. Evidence for Ca2+ entry regulated by the intracellular Ca2+ store

Sage

Reast

Rink³

1990

Biochemical Journal

153

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“…For example, synchronized calcium oscillations or intercellular calcium waves have been reported after stimulation of epithelial cells [43], hepatocytes [42] and astrocytes [21]. In all these systems, synchronization seems to be dependent primarily on the diffusion of IP 3 through gap junctions [5,21], although diffusion of calcium may also contribute to synchronization [15,20].…”

Section: Introductionmentioning

confidence: 99%

“…The role of calcium influx in intracellular calcium oscillations remains controversial. Although the presumed principal function for calcium influx during oscillations is to recharge intracellular stores and to replenish the intracellular calcium lost during oscillations [1,42], calcium entry has also been proposed to be the trigger required for repetitive calcium release [32,45].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin F2α induces unsynchronized intracellular calcium oscillations in monolayers of gap junctionally coupled NRK fibroblasts

Harks

Scheenen

Peters

et al. 2003

Pflugers Arch - Eur J Physiol

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We investigated the intracellular calcium oscillations induced by prostaglandin F2alpha (PGF2alpha) in individual cells of confluent, gap junction-coupled monolayers of normal rat kidney (NRK) fibroblasts. PGF2alpha (1000 nM) induced oscillations in more than 90% of the cells in the monolayer, but the frequency of these oscillations was highly variable between individual cells (0.2-1.4 min(-1)). The initial calcium peak resulted from calcium release from IP3-sensitive stores, while subsequent calcium transients were mediated by interplay between both IP3-sensitive calcium stores and calcium influx. The oscillation frequency was increased by sensitizing the IP3 receptor with thimerosal (10 microM) and depended on the extracellular calcium concentration. Thapsigargin (5 nM), which inhibits reuptake of calcium into the stores, only seemed to reduce the amplitude of the oscillation. Patch-clamp experiments revealed that PGF2alpha did not inhibit electrical coupling of the NRK cells in the monolayer. Gap junctional permeability of NRK cells thus appears to be sufficient to allow electrical coupling, resulting in a uniform membrane potential throughout the entire monolayer, but insufficient to synchronize the intracellular calcium oscillations upon PGF2alpha stimulation.

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“…The release of Ca 2C from the internal store is generally followed by a Ca 2C influx across the plasma membrane. The Ca 2C that enters the cells is believed to be necessary to replace Ca 2C pumped out of the cell during the period of high Ca 2C levels (Rink & Hallam 1989); it refills the intracellular stores, provides Ca 2C for long-lasting plateau signals, and also sustains repetitive Ca 2C oscillations (reviewed by Prakriya (2009)). …”

Section: Introductionmentioning

confidence: 99%

Calcium influx in mammalian eggs

Wang¹,

Macháty²

2013

Reproduction

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Calcium (Ca 2C ) signals are involved in the regulation of oocyte maturation and play a critical role during fertilization. In the egg, Ca 2C is stored in the lumen of the endoplasmic reticulum and a signal is generated when the stored Ca 2C is released through specialized channels in the membrane of the endoplasmic reticulum to elevate the free Ca 2C concentration in the cytoplasm. Extracellular Ca 2C is also important, indicated by the fact that the mobilization of luminal Ca 2C is typically followed by Ca 2C entry across the plasma membrane.The transmembrane Ca 2C flux replenishes the endoplasmic reticulum, and thus, it is essential to sustain prolonged Ca 2C signals. It also seems to be responsible for the stimulation of important signaling cascades required for complete egg activation. Characterization of the pathway that mediates Ca 2C entry implies that its major components include STIM1, a protein that senses the filling status of the stores, and ORAI1, a channel protein located in the plasma membrane. Defining the mechanism and functions of Ca 2C entry will not only lead to a better understanding of egg physiology but may also help improving the efficiency of a number of assisted reproductive technologies.Reproduction (2013) 145 R97-R105

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Calcium signalling in non-excitable cells: Notes on oscillations and store refilling

Cited by 71 publications

References 38 publications

ADP evokes biphasic Ca2+ influx in fura-2-loaded human platelets. Evidence for Ca2+ entry regulated by the intracellular Ca2+ store

ADP evokes biphasic Ca2+ influx in fura-2-loaded human platelets. Evidence for Ca2+ entry regulated by the intracellular Ca2+ store

Prostaglandin F2α induces unsynchronized intracellular calcium oscillations in monolayers of gap junctionally coupled NRK fibroblasts

Calcium influx in mammalian eggs

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