Evidence map›Paper›PMID 22633807›Full record

ArticleCurrent biology : CB2012

Transsynaptic control of presynaptic Ca²⁺ influx achieves homeostatic potentiation of neurotransmitter release.

Martin Müller, Graeme W Davis

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.5field-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

91 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. 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
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. RIM and RIM-Binding Protein Localize Synaptic CaV2 Channels to Differentially Regulate Transmission in Neuronal Circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Dlg Is Required for Short-Term Memory and Interacts with NMDAR in theInternational journal of molecular sciences · 2022
    Article
  19. Article
  20. Article

31 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

2 authors at 1 institution in 1 country.

Martin MüllerDepartment of Biochemistry & Biophysics, 1550 4(th) Street, Rock Hall 4(th) Floor North, University of California, San Francisco, San Francisco, CA 94158, USA.
Graeme W Davis
University of California, San Francisco · US

Funding

GENETIC ANALYSIS OF SYNAPTIC HOMEOSTASISR01NS039313 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2000 to 2016
$5.3M
TRANS-SYNAPTIC SIGNALING DURING NEUROMUSCULAR DEVELOPMENTR01NS059867 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2008 to 2015
$2.7M
NINDS NIH HHS NS39313NINDS NIH HHS R01 NS039313NINDS NIH HHS R01 NS059867
6 · The paper itself

Abstract

Given the complexity of the nervous system and its capacity for change, it is remarkable that robust, reproducible neural function and animal behavior can be achieved. It is now apparent that homeostatic signaling systems have evolved to stabilize neural function. At the neuromuscular junction (NMJ) of organisms ranging from Drosophila to human, inhibition of postsynaptic neurotransmitter receptor function causes a homeostatic increase in presynaptic release that precisely restores postsynaptic excitation. Here we address what occurs within the presynaptic terminal to achieve homeostatic potentiation of release at the Drosophila NMJ. By imaging presynaptic Ca(2+) transients evoked by single action potentials, we reveal a retrograde, transsynaptic modulation of presynaptic Ca(2+) influx that is sufficient to account for the rapid induction and sustained expression of the homeostatic change in vesicle release. We show that the homeostatic increase in Ca(2+) influx and release is blocked by a point mutation in the presynaptic CaV2.1 channel, demonstrating that the modulation of presynaptic Ca(2+) influx through this channel is causally required for homeostatic potentiation of release. Together with additional analyses, we establish that retrograde, transsynaptic modulation of presynaptic Ca(2+) influx through CaV2.1 channels is a key factor underlying the homeostatic regulation of neurotransmitter release.

Indexed as

Models, BiologicalAction PotentialsAnimalsCalciumCalcium Channels, N-TypeDrosophilaHomeostasisNeuromuscular JunctionNeurotransmitter AgentsPoint MutationPresynaptic TerminalsCalciumCalcium Channels, N-TypeNeurotransmitter Agents

Identifiers

PMID22633807
PMCPMC4367479
OpenAlexW1973427588

What OpenQuestion holds

Textmetadata
LicenceTDM
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.