Evidence map›Paper›PMID 12122046›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Presynaptic mitochondrial calcium sequestration influences transmission at mammalian central synapses.

Brian Billups, Ian D Forsythe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

226 citing papers in PubMed, 1 synthesis or guideline pooled it, 413 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
  6. Article
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  8. Article
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  11. Article
  12. Article
  13. Article
  14. Mitochondrial CaBiomolecules · 2026
    Review
  15. Review
  16. Review
  17. Article
  18. Neurobiology of mitochondrial dynamics in sleep.The Journal of physiology · 2025
    Review
  19. Article
  20. Article

166 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Brian BillupsDepartment of Cell Physiology and Pharmacology, University of Leicester, Leicester LE1 9HN, United Kingdom.
Ian D Forsythe
University of Leicester · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Beyond their role in generating ATP, mitochondria have a high capacity to sequester calcium. The interdependence of these functions and limited access to presynaptic compartments makes it difficult to assess the role of sequestration in synaptic transmission. We addressed this important question using the calyx of Held as a model glutamatergic synapse by combining patch-clamp with a novel mitochondrial imaging method. Presynaptic calcium current, mitochondrial calcium concentration ([Ca(2+)](mito), measured using rhod-2 or rhod-FF), cytoplasmic calcium concentration ([Ca(2+)](cyto), measured using fura-FF), and the postsynaptic current were monitored during synaptic transmission. Presynaptic [Ca(2+)](cyto) rose to 8.5 +/- 1.1 microM and decayed rapidly with a time constant of 45 +/- 3 msec; presynaptic [Ca(2+)](mito) also rose rapidly to >5 microM but decayed slowly with a half-time of 1.5 +/- 0.4 sec. Mitochondrial depolarization with rotenone and carbonyl cyanide p-trifluoromethoxyphenylhydrazone abolished mitochondrial calcium rises and slowed the removal of [Ca(2+)](cyto) by 239 +/- 22%. Using simultaneous presynaptic and postsynaptic patch clamp, combined with presynaptic mitochondrial and cytoplasmic imaging, we investigated the influence of mitochondrial calcium sequestration on transmitter release. Depletion of ATP to maintain mitochondrial membrane potential was blocked with oligomycin, and ATP was provided in the patch pipette. Mitochondrial depolarization raised [Ca(2+)](cyto) and reduced transmitter release after short EPSC trains (100 msec, 200 Hz); this effect was reversed by raising mobile calcium buffering with EGTA. Our results suggest a new role for presynaptic mitochondria in maintaining transmission by accelerating recovery from synaptic depression after periods of moderate activity. Without detectable thapsigargin-sensitive presynaptic calcium stores, we conclude that mitochondria are the major organelle regulating presynaptic calcium at central glutamatergic terminals.

Indexed as

Adenosine TriphosphateAnimalsBrain StemCalciumCalcium SignalingCytoplasmElectric StimulationEnzyme InhibitorsExcitatory Postsynaptic PotentialsFluorescent DyesGlutamic AcidIn Vitro TechniquesMitochondriaOligomycinsPatch-Clamp TechniquesPresynaptic TerminalsAdenosine TriphosphateCalciumEnzyme InhibitorsFluorescent DyesGlutamic AcidOligomycinsUncoupling Agents

Identifiers

PMID12122046
PMCPMC6757942
OpenAlexW2153456027

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.