Evidence map›Paper›PMID 9425119›Full record

ArticleThe Biochemical journal1998

Ca2+ entry into PC12 cells initiated by ryanodine receptors or inositol 1,4,5-trisphosphate receptors.

D L Bennett, M D Bootman, M J Berridge, T R Cheek

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023
    Review
  3. Review
  4. Article
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  6. STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology.American journal of physiology. Heart and circulatory physiology · 2013
    Review
  7. Article
  8. Article
  9. Review
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  11. Review
  12. Article
  13. Effects of Apigenin on Glutamate-induced [Ca](i) Increases in Cultured Rat Hippocampal Neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008
    Article
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  20. Distinct intracellular calcium transients in neurites and somata integrate neuronal signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

D L BennettThe Babraham Institute Laboratory of Molecular Signalling, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, U.K.
M D Bootman
M J Berridge
T R Cheek
University of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Capacitative Ca2+ entry (CCE) is a universal mechanism for refilling intracellular Ca2+ stores in electrically non-excitable cells. The situation in excitable cells is less clear, however, since they may rely on other entry mechanisms for Ca2+-store refilling. In the present study we investigated CCE in intact PC12 cells, using acetylcholine to bring about activation of InsP3 receptors (InsP3Rs), caffeine to activate ryanodine receptors (RyRs) and thapsigargin to inhibit sarco/endoplasmic reticulum Ca2+-ATPase pumps. We found that depletion of the InsP3-, caffeine- or thapsigargin-sensitive stores promoted Ca2+ entry, suggesting that stimulation of either InsP3Rs or RyRs can activate CCE. The CCE pathways activated by InsP3Rs, RyRs and thapsigargin appeared to be independent at least in part, since their effects were found to be additive. However, CCE triggered by caffeine, acetylcholine or thapsigargin progressively diminished with time. The decay of CCE caused by one agent also inhibited subsequent responses to the others, suggesting that some component of the CCE pathway is common to all intracellular Ca2+ stores. The magnitude of CCE stimulated by InsP3Rs or RyRs was related to the size of the stores; the InsP3-sensitive store was smaller than the RyR-sensitive store and triggered a smaller entry component. However, both stores filled with a similar half time (about 1 min), and both could be filled more rapidly by depolarization-induced Ca2+ entry through voltage-operated channels. A significant basal Ca2+ influx was apparent in PC12 cells. The basal entry component may be under the control of the InsP3-sensitive Ca2+ store, since short incubations in Ca2+-free medium depleted this store.

Indexed as

AcetylcholineAnimalsCaffeineCalciumCalcium ChannelsInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsIon TransportPC12 CellsRatsReceptors, Cytoplasmic and NuclearRyanodine Receptor Calcium Release ChannelThapsigarginAcetylcholineCaffeineCalciumCalcium ChannelsInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsReceptors, Cytoplasmic and NuclearRyanodine Receptor Calcium Release ChannelThapsigargin

Identifiers

PMID9425119
PMCPMC1219051
OpenAlexW1513064825

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.