Evidence map›Paper›PMID 26804996›Full record

ArticleNeuron2016

IGF-1 Receptor Differentially Regulates Spontaneous and Evoked Transmission via Mitochondria at Hippocampal Synapses.

Neta Gazit, Irena Vertkin, Ilana Shapira, Martin Helm, Edden Slomowitz, Maayan Sheiba, Yael Mor, Silvio Rizzoli, Inna Slutsky

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
9.7field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 141 citations in OpenAlex.

  1. Neurological Effects ofNutrients · 2026
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  3. Mitochondrial CaNature metabolism · 2026
    Article
  4. Review
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  6. Review
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  9. Review
  10. Review
  11. Review
  12. Disease-relevant upregulation of P2YNature communications · 2024
    Article
  13. A role for astrocytic insulin-like growth factor I receptors in the response to ischemic insult.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Mitochondria as central hubs in synaptic modulation.Cellular and molecular life sciences : CMLS · 2023
    Review

22 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

9 authors at 3 institutions in 2 countries.

Neta GazitDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, 69978 Tel Aviv, Israel.
Irena VertkinDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel.
Ilana ShapiraDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel.
Martin HelmDepartment of Neuro- and Sensory Physiology, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, European Neuroscience Institute, University of Göttingen Medical Center, 37075 Göttingen, Germany; International Max Planck Research School Molecular Biology, 37077 Göttingen, Germany.
Edden SlomowitzDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel.
Maayan SheibaDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel.
Yael MorDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, 69978 Tel Aviv, Israel.
Silvio RizzoliDepartment of Neuro- and Sensory Physiology, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, European Neuroscience Institute, University of Göttingen Medical Center, 37075 Göttingen, Germany.
Inna SlutskyDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, 69978 Tel Aviv, Israel. Electronic address: islutsky@post.tau.ac.il.
Tel Aviv University · ILNanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DEUniversity of Göttingen · DE

Funding

European Research Council 281403
6 · The paper itself

Abstract

The insulin-like growth factor-1 receptor (IGF-1R) signaling is a key regulator of lifespan, growth, and development. While reduced IGF-1R signaling delays aging and Alzheimer's disease progression, whether and how it regulates information processing at central synapses remains elusive. Here, we show that presynaptic IGF-1Rs are basally active, regulating synaptic vesicle release and short-term plasticity in excitatory hippocampal neurons. Acute IGF-1R blockade or transient knockdown suppresses spike-evoked synaptic transmission and presynaptic cytosolic Ca(2+) transients, while promoting spontaneous transmission and resting Ca(2+) level. This dual effect on transmitter release is mediated by mitochondria that attenuate Ca(2+) buffering in the absence of spikes and decrease ATP production during spiking activity. We conclude that the mitochondria, activated by IGF-1R signaling, constitute a critical regulator of information processing in hippocampal neurons by maintaining evoked-to-spontaneous transmission ratio, while constraining synaptic facilitation at high frequencies. Excessive IGF-1R tone may contribute to hippocampal hyperactivity associated with Alzheimer's disease.

Indexed as

Adenosine TriphosphateAnimalsCalciumCells, CulturedExcitatory Postsynaptic PotentialsHippocampusInsulin-Like Growth Factor IMiceMiniature Postsynaptic PotentialsMitochondriaNeuronal PlasticityNeuronsPresynaptic TerminalsPrimary Cell CultureReceptor, IGF Type 1Signal TransductionAdenosine TriphosphateCalciumInsulin-Like Growth Factor IReceptor, IGF Type 1

Identifiers

PMID26804996
PMCPMC4742535
OpenAlexW2272398100

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.