Occurrence of Na+–Ca2+exchange in the ciliateEuplotes crassusand its role in Ca2+homeostasis

Burlando, Bruno; Malinowska, Barbara; Krüppel, Thomas; Orunesu, M; Viarengo, Aldo

doi:10.1054/ceca.1998.0014

Cited by 16 publications

(14 citation statements)

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“…However, the electrochemical gradient of the Ca ++ ions would be steeper than that of K + ions (the potential at equilibrium of K + is -68 mV); hence the ion flow would be directed inside a cell and produce a new depolarisation. Also, according to observations of Burlando et al (1999), the toxin would prevent the compensatory mechanism due to the effects of ions on the cell membrane voltage. Supposing that the ionophore is analogous to the Ca ++ channels (third possibility), then Ca ++ would follow their gradient, and the membrane would be depolarised.…”

Section: Discussionmentioning

confidence: 98%

Action ofLitonotus(predator) toxicysts on the electric properties ofEuplotes(prey) cell membrane

Morelli

Ricci

Verni

2002

Italian Journal of Zoology

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The effects of toxicyst discharge by the predator, Litonotus lamella, on the cell membrane of the prey, Euplotes vannus, were studied electrophysiologically. Euplotes specimens were penetrated with a microelectrode filled with a 1 M KC1 solution to measure: (i) the spontaneous fluctuations of their membrane potential, (ii) the responses of their membrane to current stimuli, and (iii) the cell membrane input resistance before, during, and after their contact with the predator. It was found that: (a) when a Euplotes was struck by Litonotus toxicysts, the membrane potential shifted from a resting value of -35 mV up to -5 mV, and then it slowly repolarised to -20 mV and depolarised again very slowly toward 0 mV, (b) the cell membrane gave only passive responses to injections of current and the input resistance decreased, (c) an inward current was responsible for the sudden depolarisation previously described. The conclusion drawn from these observations is that the toxin(s) released from the toxicysts of Litonotus affects the plasma membrane potential of Euplotes by activating all the ion channels simultaneously.

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Section: Discussionmentioning

confidence: 98%

Action ofLitonotus(predator) toxicysts on the electric properties ofEuplotes(prey) cell membrane

Morelli

Ricci

Verni

2002

Italian Journal of Zoology

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“…(iii) While we routinely exclude mechanical activation during secretion activation (not shown here; see Erxleben & Plattner [15]), activation of either type of cation channel or of any other unidentified type, possibly of some Ca channels still to be specified [46,47] or via a newly discovered Na + /Ca 2+ exchanger in ciliates [6] would appear feasible or, at least, cannot be excluded. Can the number of candidates be restricted?…”

Section: Discussionmentioning

confidence: 99%

Veratridine-Mediated Ca 2+ Dynamics and Exocytosis in Paramecium Cells

Blanchard

Klauke

Zitzmann

et al. 1999

Journal of Membrane Biology

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“…In the heart muscle sarcolemma, a Ca 2+ /Na + antiporter (exchanger) supports this ongoing activity, with sodium being equilibrated by a secondary active transport process. Although claimed also for ciliates (Burlando et al 1999), such activity could not be convincingly ascertained.…”

Section: Ca 2+ Extrusion At the Cell Surfacementioning

confidence: 93%

“…Although claimed also for ciliates (Burlando et al. ), such activity could not be convincingly ascertained.…”

Section: Capabilities Of Ca2+ Signaling From Paramecium To Manmentioning

confidence: 96%

Calcium Regulation in the Protozoan Model, Paramecium tetraurelia

Plattner

2013

J Eukaryotic Microbiology

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Early in eukaryotic evolution, the cell has evolved a considerable inventory of proteins engaged in the regulation of intracellular Ca(2+) concentrations, not only to avoid toxic effects but beyond that to exploit the signaling capacity of Ca(2+) by small changes in local concentration. Among protozoa, the ciliate Paramecium may now be one of the best analyzed models. Ciliary activity and exo-/endocytosis are governed by Ca(2+) , the latter by Ca(2+) mobilization from alveolar sacs and a superimposed store-operated Ca(2+) -influx. Paramecium cells possess plasma membrane- and endoplasmic reticulum-resident Ca(2+) -ATPases/pumps (PMCA, SERCA), a variety of Ca(2+) influx channels, including mechanosensitive and voltage-dependent channels in the plasma membrane, furthermore a plethora of Ca(2+) -release channels (CRC) of the inositol 1,4,5-trisphosphate and ryanodine receptor type in different compartments, notably the contractile vacuole complex and the alveolar sacs, as well as in vesicles participating in vesicular trafficking. Additional types of CRC probably also occur but they have not been identified at a molecular level as yet, as is the equivalent of synaptotagmin as a Ca(2+) sensor for exocytosis. Among established targets and sensors of Ca(2+) in Paramecium are calmodulin, calcineurin, as well as Ca(2+) /calmodulin-dependent protein kinases, all with multiple functions. Thus, basic elements of Ca(2+) signaling are available for Paramecium.

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Occurrence of Na+–Ca2+exchange in the ciliateEuplotes crassusand its role in Ca2+homeostasis

Cited by 16 publications

References 0 publications

Action ofLitonotus(predator) toxicysts on the electric properties ofEuplotes(prey) cell membrane

Action ofLitonotus(predator) toxicysts on the electric properties ofEuplotes(prey) cell membrane

Veratridine-Mediated Ca 2+ Dynamics and Exocytosis in Paramecium Cells

Calcium Regulation in the Protozoan Model, Paramecium tetraurelia

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