Evidence map›Paper›PMID 36274588›Full record

ArticleJournal of cell science2022

Mitochondrial Ca2+ uniporter haploinsufficiency enhances long-term potentiation at hippocampal mossy fibre synapses.

Michael J Devine, Blanka R Szulc, Jack H Howden, Guillermo López-Doménech, Arnaud Ruiz, Josef T Kittler

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Mitochondrial CaNature metabolism · 2026
    Article
  4. Mitochondrial CaBiomolecules · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Mitofusin 2 Sustains the Axonal Mitochondrial Network to Support Presynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  15. Mitochondrial CaBiomedicines · 2022
    Review
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

6 authors at 1 institution in 1 country.

Michael J DevineDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.ORCID 0000-0001-6076-3382
Blanka R SzulcDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
Jack H HowdenDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.ORCID 0000-0001-9303-2076
Guillermo López-DoménechDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
Arnaud RuizDepartment of Pharmacology, School of Pharmacy, University College London, Brunswick Square, London WC1N 1AX, UK.ORCID 0000-0001-9058-9303
Josef T KittlerDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.ORCID 0000-0002-3437-9456
University College London · GB

Funding

European Research Council 282430Wellcome TrustWellcome Trust 106713/Z/14/Z
6 · The paper itself

Abstract

Long-term changes in synaptic strength form the basis of learning and memory. These changes rely upon energy-demanding mechanisms, which are regulated by local Ca2+ signalling. Mitochondria are optimised for providing energy and buffering Ca2+. However, our understanding of the role of mitochondria in regulating synaptic plasticity is incomplete. Here, we have used optical and electrophysiological techniques in cultured hippocampal neurons and ex vivo hippocampal slices from mice with haploinsufficiency of the mitochondrial Ca2+ uniporter (MCU+/-) to address whether reducing mitochondrial Ca2+ uptake alters synaptic transmission and plasticity. We found that cultured MCU+/- hippocampal neurons have impaired Ca2+ clearance, and consequently enhanced synaptic vesicle fusion at presynapses occupied by mitochondria. Furthermore, long-term potentiation (LTP) at mossy fibre (MF) synapses, a process which is dependent on presynaptic Ca2+ accumulation, is enhanced in MCU+/- slices. Our results reveal a previously unrecognised role for mitochondria in regulating presynaptic plasticity of a major excitatory pathway involved in learning and memory.

Indexed as

Long-Term PotentiationMossy Fibers, HippocampalAnimalsCalciumHaploinsufficiencyMiceMitochondriaSynapsesSynaptic TransmissionCalciumCa2+Long-term potentiationMCUMitochondriaMossy fibre synapse

Identifiers

PMID36274588
PMCPMC10563808
OpenAlexW4307178596

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.