Evidence map›Paper›PMID 10531430›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Mitochondria regulate the Ca(2+)-exocytosis relationship of bovine adrenal chromaffin cells.

D R Giovannucci, M D Hlubek, E L Stuenkel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
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  8. Article
  9. Regulation by L-type calcium channels of endocytosis: an overview.Journal of molecular neuroscience : MN · 2012
    Review
  10. Permissive role of sphingosine on calcium-dependent endocytosis in chromaffin cells.Pflugers Archiv : European journal of physiology · 2010
    Article
  11. Article
  12. Mitochondria modulate Ca2+-dependent glutamate release from rat cortical astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  19. Article
  20. Presynaptic mitochondrial calcium sequestration influences transmission at mammalian central synapses.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

3 authors at 1 institution in 1 country.

D R GiovannucciDepartment of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0622, USA. giovannucci@pharmacol.rochester.edu
M D Hlubek
E L Stuenkel
University of Michigan–Ann Arbor · US

Funding

SNARE HYPOTHESIS AT NERVE ENDINGSR01NS036227 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STUENKEL, EDWARD L · 1998 to 2002
$659k
NINDS NIH HHS NS36227
6 · The paper itself

Abstract

The present study expands the contemporary view of mitochondria as important participants in cellular Ca(2+) dynamics and provides evidence that mitochondria regulate the supply of release-competent secretory granules. Using pharmacological probes to inhibit mitochondrial Ca(2+) import, the ability of mitochondria to modulate secretory activity in single, patch-clamped bovine chromaffin cells was examined by simultaneously monitoring rapid changes in membrane surface area (DeltaC(m)) and cytosolic Ca(2+) levels ([Ca(2+)](c)). Repetitive step depolarizations or action potential waveforms were found to raise the [Ca(2+)](c) of chromaffin cells into the 1 microM to tens of micromolar range. Inhibiting mitochondria by treatment with carbonyl cyanide p-(trifuoro-methoxy)phenylhydrazone, antimycin-oligomycin, or ruthenium red revealed that mitochondria are a prominent component for the clearance of Ca(2+) that entered via voltage-activated Ca(2+) channels. Disruption of cellular Ca(2+) homeostasis by poisoning mitochondria enhanced the secretory responsiveness of chromaffin cells by increasing the amplitude of the transient rise and the time course of recovery to baseline of the evoked Delta[Ca(2+)](c). The enhancement of the secretory response was represented by significant deviation of the Ca(2+)-exocytosis relationship from a standard relationship that equates Ca(2+) influx and DeltaC(m). Thus, mitochondria would play a critical role in the control of secretory activity in chromaffin cells that undergo tonic or repetitive depolarizing activity, likely by limiting the Ca(2+)-dependent activation of specific proteins that recruit or prime secretory granules for exocytosis.

Indexed as

Action PotentialsAdrenal CortexAnimalsCadmiumCalciumCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCattleCells, CulturedChromaffin CellsDimethylphenylpiperazinium IodideEgtazic AcidExocytosisKineticsMembrane PotentialsMitochondriaPatch-Clamp TechniquesCadmiumCalciumCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneDimethylphenylpiperazinium IodideEgtazic Acid

Identifiers

PMID10531430
PMCPMC6782892
OpenAlexW1675974676

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.