Evidence map›Paper›PMID 25151265›Full record

ArticleNature neuroscience2014

Activity-dependent regulation of astrocyte GAT levels during synaptogenesis.

Allie K Muthukumar, Tobias Stork, Marc R Freeman

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

87 citing papers in PubMed, 143 citations in OpenAlex.

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  15. Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024
    Review
  16. Article
  17. Fly into tranquility: GABA's role in Drosophila sleep.Current opinion in insect science · 2024
    Review
  18. Article
  19. Article
  20. Article

27 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

3 authors at 1 institution in 1 country.

Allie K Muthukumar1] Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [2] Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Tobias Stork1] Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [2] Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Marc R Freeman1] Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [2] Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
University of Massachusetts Chan Medical School · US

Funding

Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
The Draper signaling pathway in Drosophila glial immune functionsR01NS053538 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Marc R Freeman · 2006 to 2026
$5.3M
Transmission Electron Microscope for Core EM FacilityS10RR027897 · NCRR · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CRAIG, ROGER W · 2009 to 2009
$500k
Howard Hughes Medical InstituteNCRR NIH HHS S10RR027897NIGMS NIH HHS R01 GM084947NIGMS NIH HHS R01-GM084947NINDS NIH HHS R01 NS053538NINDS NIH HHS R01NS053538
6 · The paper itself

Abstract

Astrocytic uptake of GABA through GABA transporters (GATs) is an important mechanism regulating excitatory/inhibitory balance in the nervous system; however, mechanisms by which astrocytes regulate GAT levels are undefined. We found that at mid-pupal stages the Drosophila melanogaster CNS neuropil was devoid of astrocyte membranes and synapses. Astrocyte membranes subsequently infiltrated the neuropil coordinately with synaptogenesis, and astrocyte ablation reduced synapse numbers by half, indicating that Drosophila astrocytes are pro-synaptogenic. Shortly after synapses formed in earnest, GAT was upregulated in astrocytes. Ablation or silencing of GABAergic neurons or disruption of metabotropic GABA receptor 1 and 2 (GABA(B)R1/2) signaling in astrocytes led to a decrease in astrocytic GAT. Notably, developmental depletion of astrocytic GABA(B)R1/2 signaling suppressed mechanosensory-induced seizure activity in mutants with hyperexcitable neurons. These data reveal that astrocytes actively modulate GAT expression via metabotropic GABA receptor signaling and highlight the importance of precise regulation of astrocytic GAT in modulation of seizure activity.

Indexed as

Analysis of VarianceAnimalsAnimals, Genetically ModifiedAstrocytesDrosophilaDrosophila ProteinsGABAergic NeuronsLuminescent ProteinsMicroscopy, ConfocalMicroscopy, Electron, TransmissionNeurogenesisNeuronsParalysisPeptidesPhysical StimulationPolymersDrosophila ProteinsGAL4 protein, DrosophilaGATLuminescent ProteinsPeptidesPolymersTranscription Factors

Identifiers

PMID25151265
PMCPMC4176984
OpenAlexW1976458700

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.