Evidence map›Paper›PMID 32729828›Full record

ArticleeLife2020

A unified computational model for cortical post-synaptic plasticity.

Tuomo Mäki-Marttunen, Nicolangelo Iannella, Andrew G Edwards, Gaute T Einevoll, Kim T Blackwell

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 55 citations in OpenAlex.

  1. ICER-Controlled inhibitory plasticity of amygdala engram neurons regulates fear memory precision.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Article
  4. Pre- and Post-synaptic Mechanisms of Neuronal Inhibition Assessed Through Biochemically Detailed Modeling of GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. The plasticity of pyramidal neurons in the behaving brain.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Adaptive control of synaptic plasticity integrates micro- and macroscopic network function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 3 institutions in 2 countries.

Tuomo Mäki-MarttunenSimula Research Laboratory, Oslo, Norway.ORCID https://orcid.org/0000-0002-7082-2507
Nicolangelo IannellaDepartment of Biosciences, University of Oslo, Oslo, Norway.
Andrew G EdwardsSimula Research Laboratory, Oslo, Norway.
Gaute T EinevollFaculty of Science and Technology, Norwegian University of Life Sciences, Oslo, Norway.ORCID http://orcid.org/0000-0002-5425-5012
Kim T BlackwellThe Krasnow Institute for Advanced Study, George Mason University, Fairfax, United States.ORCID http://orcid.org/0000-0003-4711-2344
Simula Research Laboratory · NOUniversity of Oslo · NOGeorge Mason University · US

Funding

European Union Horizon 2020 Research and Innovation 785907Horizon 2020 - Research and Innovation Framework Programme 785907Research council of Norway 248828Research Council of Norway 248828
6 · The paper itself

Abstract

Signalling pathways leading to post-synaptic plasticity have been examined in many types of experimental studies, but a unified picture on how multiple biochemical pathways collectively shape neocortical plasticity is missing. We built a biochemically detailed model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic potentiation or depression. We developed a statistical AMPA-receptor-tetramer model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR2s predicted by the biochemical signalling model. We show that our model reproduces neuromodulator-gated spike-timing-dependent plasticity as observed in the visual cortex and can be fit to data from many cortical areas, uncovering the biochemical contributions of the pathways pinpointed by the underlying experimental studies. Our model explains the dependence of different forms of plasticity on the availability of different proteins and can be used for the study of mental disorder-associated impairments of cortical plasticity.

Indexed as

Neuronal PlasticitySignal TransductionAnimalsComputational BiologyMiceModels, NeurologicalRatsReceptors, AMPAVisual CortexReceptors, AMPAbiochemically detailed modelcalcium signallingcomputational biologyintracellular signalling cascadeLTP/LTDmouseneuroscienceratSTDPsystems biology

Identifiers

PMID32729828
PMCPMC7426095
OpenAlexW3047357274

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.