Evidence map›Paper›PMID 34910905›Full record

ArticleCell reports2021

Distinct molecular pathways govern presynaptic homeostatic plasticity.

Anu G Nair, Paola Muttathukunnel, Martin Müller

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Activity-Dependent Increases in Quantal Size at theJournal of developmental biology · 2025
    Article
  3. Article
  4. Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Behavioral resilience via dynamic circuit firing homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Article
  9. Precise mapping of one classic and three novelmicroPublication biology · 2023
    Article
  10. Article
  11. Rapid homeostatic modulation of transsynaptic nanocolumn rings.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. 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

3 authors at 2 institutions in 2 countries.

Anu G NairDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Department of Neuroscience, Karolinska Institute, 17177 Stockholm, Sweden.
Paola MuttathukunnelDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Neuroscience Center Zurich, University of Zurich/ETH Zurich, 8057 Zurich, Switzerland.
Martin MüllerDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Neuroscience Center Zurich, University of Zurich/ETH Zurich, 8057 Zurich, Switzerland. Electronic address: martin.mueller@mls.uzh.ch.
University of Zurich · CHETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Presynaptic homeostatic plasticity (PHP) stabilizes synaptic transmission by counteracting impaired neurotransmitter receptor function through neurotransmitter release potentiation. PHP is thought to be triggered by impaired receptor function and to involve a stereotypic signaling pathway. However, here we demonstrate that different receptor perturbations that similarly reduce synaptic transmission result in different responses at the Drosophila neuromuscular junction. While receptor inhibition by the glutamate receptor (GluR) antagonist γ-D-glutamylglycine (γDGG) is not compensated by PHP, the GluR inhibitors Philanthotoxin-433 (PhTx) and Gyki-53655 (Gyki) induce compensatory PHP. Intriguingly, PHP triggered by PhTx and Gyki involve separable signaling pathways, including inhibition of distinct GluR subtypes, differential modulation of the active-zone scaffold Bruchpilot, and short-term plasticity. Moreover, while PHP upon Gyki treatment does not require genes promoting PhTx-induced PHP, it involves presynaptic protein kinase D. Thus, synapses not only respond differentially to similar activity impairments, but achieve homeostatic compensation via distinct mechanisms, highlighting the diversity of homeostatic signaling.

Indexed as

HomeostasisNeuronal PlasticitySynaptic TransmissionAnimalsDrosophila melanogasterDrosophila ProteinsExcitatory Postsynaptic PotentialsNeuromuscular JunctionNeurotransmitter AgentsPresynaptic TerminalsReceptors, GlutamateSignal TransductionSynapsesDrosophila ProteinsNeurotransmitter AgentsReceptors, GlutamateDrosophila neuromuscular junctionglutamate receptorshomeostatic plasticityneurotransmitter releaseProtein Kinase Dsynaptic transmission

Identifiers

PMID34910905
PMCPMC8692748
OpenAlexW4225688966

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.