Evidence map›Paper›PMID 32256317›Full record

ArticleFrontiers in cellular neuroscience2020

Hebbian and Homeostatic Synaptic Plasticity-Do Alterations of One Reflect Enhancement of the Other?

Christos Galanis, Andreas Vlachos

Abstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Long-term potentiation and long-term depression are both impaired afterBiomedical physics & engineering express · 2025
    Article
  3. Article
  4. Review
  5. TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Anxiety and depression: A top-down, bottom-up model of circuit function.Annals of the New York Academy of Sciences · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Postsynaptic Potential Energy as Determinant of Synaptic Plasticity.Frontiers in computational neuroscience · 2022
    Article
  16. Article
  17. Review
  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

2 authors.

Christos GalanisDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Andreas VlachosDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the past 50 years, the cellular and molecular mechanisms of synaptic plasticity have been studied in great detail. A plethora of signaling pathways have been identified that account for synaptic changes based on positive and negative feedback mechanisms. Yet, the biological significance of Hebbian synaptic plasticity (= positive feedback) and homeostatic synaptic plasticity (= negative feedback) remains a matter of debate. Specifically, it is unclear how these opposing forms of plasticity, which share common downstream mechanisms, operate in the same networks, neurons, and synapses. Based on the observation that rapid and input-specific homeostatic mechanisms exist, we here discuss a model that is based on signaling pathways that may adjust a balance between Hebbian and homeostatic synaptic plasticity. Hence, "alterations" in Hebbian plasticity may, in fact, resemble "enhanced" homeostasis, which rapidly returns synaptic strength to baseline. In turn, long-lasting experience-dependent synaptic changes may require attenuation of homeostatic mechanisms or the adjustment of homeostatic setpoints at the single-synapse level. In this context, we propose a role for the proteolytic processing of the amyloid precursor protein (APP) in setting a balance between the ability of neurons to express Hebbian and homeostatic synaptic plasticity.

Indexed as

amyloid precursor proteinamyloid-βAPPsαBACE1hebbian plasticityhomeostatic plasticitysynaptic scaling

Identifiers

PMID32256317
PMCPMC7093376

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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.