Measurement of cytosolic free Ca<sup>2+</sup> in individual pancreatic acini

Pralong, William; Wollheim, Claes B.; Bruzzone, Roberto

doi:10.1016/0014-5793(88)80989-x

Cited by 49 publications

(19 citation statements)

References 33 publications

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“…ed oscillations have l'eC¢lltly bCell t'eportcd to occur in bovine puhuonary artery end¢~thclial [16], rat aortic ,~mooth muscle [18], and pancreatic aci.ar cell popula. lions [19], Since we have found theft spiki.t beluwiour occurs only in confluent ceils, .rid is not seen in cith~r pre. or l:~Ost.cot~fhtent monolayers, synchremized spik.…”

Section: Discussionmentioning

confidence: 61%

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Neylon

Irvine

1990

FEBS Letters

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Synchronized repetitive spikes in cytoplasmic free calcium concentration, [Ca2+]i, are evoked by histamine in confluent monolayers of human endothelial cells. The repetitive spikes, which are apparently dependent upon the establishment of cell coupling, are also induced by caffeine, indicating that they may be due to an oscillatory release of Ca2+ from the endoplasmic reticulum, and may not involve oscillations in inositol phosphates. It is suggested that sunchronized repetitive spikes in [Ca2+]i might lead to oscillatory release of endothelial‐derived substances such as prostacyclin, nitric oxide and endothelin, which have potent effects on the vascular system.

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Section: Discussionmentioning

confidence: 61%

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Neylon

Irvine

1990

FEBS Letters

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“…It is also well known that CCK and its active analogues can evoke an increase in [Ca2+]i in pancreatic acinar cells (Schulz, 1980;Muallem, 1989). Oscillations in [Ca2+]j in response to the CCK analogue caerulein were recently demonstrated in isolated rat pancreatic acini (Pralong et al, 1988). Figure 5 shows the effect of 10 nM CCK on [Ca2 ]i assessed by fura-2 microfluorimetry and Ca2+ dependent Clcurrent recording.…”

Section: Resultsmentioning

confidence: 86%

“…Extensive intracellular microelectrode studies on mouse pancreatic acini show that activations of the distinct ACh and CCK receptors evoke opening of the same conductance pathways (Petersen, 1973;Nishiyama and Petersen, 1974;Petersen and Ueda, 1975). It is also well known that CCK and its active analogues can evoke an increase in [Ca2+]i in pancreatic acinar cells (Schulz, 1980;Muallem, 1989 (Pralong et al, 1988). Clcurrent recording.…”

Section: Resultsmentioning

confidence: 99%

Cytoplasmic Ca2+ oscillations evoked by receptor stimulation, G-protein activation, internal application of inositol trisphosphate or Ca2+: simultaneous microfluorimetry and Ca2+ dependent Cl- current recording in single pancreatic acinar cells.

et al. 1990

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The effects of acetylcholine (ACh), cholecystokinin (CCK), internally applied GTP‐gamma‐S, inositol trisphosphate [Ins (1,4,5) P3] or Ca2+ on the cytoplasmic free Ca2+ concentration [( Ca2+]i) were assessed by simultaneous microfluorimetry (fura‐2) and measurement of the Ca2(+)‐dependent Cl‐ current (patch‐clamp whole‐cell recording) in single internally perfused mouse pancreatic acinar cells. ACh (0.1‐0.2 microM) evoked an oscillating increase in [Ca2+]i measured in the cell as a whole (microfluorimetry) which was synchronous with oscillations in the Ca2(+)‐dependent Cl‐ current reporting [Ca2+]i close to the cell membrane. In the same cells a lower ACh concentration (0.05 microM) evoked shorter repetitive Cl‐ current pulses that were not accompanied by similar spikes in the microfluorimetric recording. When cells did not respond to 0.1 microM ACh, caffeine (1 mM) added on top of the sustained ACh stimulus resulted in [Ca2+]i oscillations seen synchronously in both types of recording. CCK (10 nM) also evoked [Ca2+]i oscillations, but with much longer intervals between slightly broader Ca2+ pulses. Internal perfusion with 100 microM GTP‐gamma‐S evoked [Ca2+]i oscillations with a similar pattern. Ins (1,4,5) P3 (10 microM) evoked repetitive shortlasting spikes in [Ca2+]i that were only seen in the Cl‐ current traces, except in one small cell where these spikes were also observed synchronously in the microfluorimetric recording. Caffeine (1 mM) broadened these Ca2+ pulses. [Ca2+]i was also directly changed, bypassing the normal signalling process, by infusion of a low or high Ca2+ solution into the pipette.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Synchronised Ca2+ oscillations have also been shown in monolayers of endothelial cells [28][29][30], in electrically active pancreatic p-cells [7,31] and in human sweat gland epithelial cells [32]. In most cases, the underlying mechanism was unknown.…”

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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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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Measurement of cytosolic free Ca²⁺ in individual pancreatic acini

Cited by 49 publications

References 33 publications

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Cytoplasmic Ca2+ oscillations evoked by receptor stimulation, G-protein activation, internal application of inositol trisphosphate or Ca2+: simultaneous microfluorimetry and Ca2+ dependent Cl- current recording in single pancreatic acinar cells.

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

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Measurement of cytosolic free Ca2+ in individual pancreatic acini

Cited by 49 publications

References 33 publications

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Synchronized repetitive spikes in cytoplasmic calcium in confluent monolayers of human umbilical vein endothelial cells

Cytoplasmic Ca2+ oscillations evoked by receptor stimulation, G-protein activation, internal application of inositol trisphosphate or Ca2+: simultaneous microfluorimetry and Ca2+ dependent Cl- current recording in single pancreatic acinar cells.

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

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Measurement of cytosolic free Ca²⁺ in individual pancreatic acini