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Cited by 23Ion Channels and ReceptorsIon channel regulation and functionCalcium signaling and nucleotide metabolism

Voltage-dependent Ba2+ permeation through store-operated CRAC channels: Implications for channel selectivity

Bakowski, Daniel, Parekh, Anant B.·2007·Cell Calcium
DOI 10.1016/j.ceca.2007.01.005
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Abstract

Store-operated Ca2+ entry through CRAC channels is a major route for Ca2+ influx in non-excitable cells. Studies on store-operated channel selectivity using fluorescent dyes have found that the channels are impermeable to Ba2+. Furthermore, in such studies, agonists have been reported to increase Ba2+ influx, leading to the conclusion that additional Ca2+ entry pathways (permeable to Ba2+) co-exist with the Ba2+-impermeable store-operated channels. However, patch clamp experiments demonstrate that CRAC channels are permeable to Ba2+. We have addressed this paradox using fluorescence measurements and whole cell patch clamp recordings of ICRAC. In store-depleted cells loaded with fura 2, Ba2+ application results in a slower and smaller rise in fluorescence than is the case with Ca2+. Ba2+, unlike Ca2+, depolarises the membrane potential by approximately 40 mV, due to rapid block of an inwardly rectifying K+ current. Although Ba2+ permeates CRAC channels at very negative potentials in patch clamp recordings, Ba2+ permeation is steeply voltage-dependent. This combination of Ba2+-dependent depolarisation and voltage-dependent Ba2+ permeation accounts for the apparent lack of Ba2+ permeation through store-operated channels seen in fluorescence experiments. Our findings identify major limitations with the use of Ba2+ as a surrogate for Ca2+ in probing Ca2+ entry pathways and raise the possibility that some of the previous reports proposing multiple Ca2+ entry pathways based on Ba2+ entry into fura 2-loaded cells could be explained by voltage-dependent Ba2+ permeation through CRAC channels.

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Crossref · 10.1016/j.ceca.2007.01.005

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  • CRAC channels also exhibit a similar voltage-dependent influx of Ba2+ at negative membrane potentials.

    “Interestingly, CRAC channels, a subtype of the voltage-independent SOC channels in mammalian cells, also exhibit a similar voltage-dependent influx of Ba 2ϩ at negative membrane potentials (34).”

    From Cch1 Restores Intracellular Ca2+ in Fungal Cells during Endoplasmic Reticulum Stress (2010) · cites this paper as [34]

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Authors
Bakowski, D., & Parekh, A. B.
Affiliations
University of Oxford (GB)
Corresponding author
Parekh, Anant B.
ORCID
Parekh, Anant B.
Venue
Cell Calcium
Publisher
Elsevier BV
Published
2007-09
Volume
42
Issue
3
Pages
333-339
ISSN
0143-4160 (ISSN-L)
DOI
10.1016/j.ceca.2007.01.005
OpenAlex
W1989019725
Cited by
23
References
27
Citations by year
2026: 1 · 2025: 1 · 2021: 1 · 2019: 2 · 2018: 1 · 2016: 1 · 2014: 1 · 2013: 1 · 2012: 3
FWCI
1.54
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Cell Calcium (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Lister Institute of Preventive Medicine
  • Mauritius Research Council
Topics
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
store-operated calcium entry, CRAC channels, channel selectivity, inward rectifier potassium current, membrane depolarization, fura-2 fluorescence, store depletion
MeSH terms
Animals, Barium, Calcium, Cell Line, Fluorescent Dyes, Membrane Potentials, Calcium Channels, Potassium Channels, Ion Channel Gating, Fura-2, Patch-Clamp Techniques

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