Evidence map›Paper›PMID 28186121›Full record

ArticleNature communications2017

Astrocyte deletion of Bmal1 alters daily locomotor activity and cognitive functions via GABA signalling.

Olga Barca-Mayo, Meritxell Pons-Espinal, Philipp Follert, Andrea Armirotti, Luca Berdondini, Davide De Pietri Tonelli

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
8.1field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 216 citations in OpenAlex.

  1. Article
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  8. REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Deletion of Clock GeneClocks & sleep · 2025
    Article
  16. Bmal1 Modulates Striatal cAMP Signaling and Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  17. Article
  18. Astrocytes Regulate Brain State Transitions.Neurochemical research · 2025
    Review
  19. Review
  20. Review

65 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

6 authors at 1 institution in 1 country.

Olga Barca-MayoNeurobiology of miRNA Lab, Neuroscience and Brain Technologies Department, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.
Meritxell Pons-EspinalNeurobiology of miRNA Lab, Neuroscience and Brain Technologies Department, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.
Philipp FollertNeurobiology of miRNA Lab, Neuroscience and Brain Technologies Department, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.
Andrea ArmirottiD3 PharmaChemistry, Department of Drug Discovery and Development, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.
Luca BerdondiniNetS3 Lab, Neuroscience and Brain Technologies Department, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.ORCID 0000-0001-9521-2812
Davide De Pietri TonelliNeurobiology of miRNA Lab, Neuroscience and Brain Technologies Department, Fondazione Istituto Italiano di Tecnologia, Via Morego 30, 16163 Genoa, Italy.ORCID 0000-0001-9537-8900
Italian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circadian rhythms are controlled by a network of clock neurons in the central pacemaker, the suprachiasmatic nucleus (SCN). Core clock genes, such as Bmal1, are expressed in SCN neurons and in other brain cells, such as astrocytes. However, the role of astrocytic clock genes in controlling rhythmic behaviour is unknown. Here we show that ablation of Bmal1 in GLAST-positive astrocytes alters circadian locomotor behaviour and cognition in mice. Specifically, deletion of astrocytic Bmal1 has an impact on the neuronal clock through GABA signalling. Importantly, pharmacological modulation of GABAA-receptor signalling completely rescues the behavioural phenotypes. Our results reveal a crucial role of astrocytic Bmal1 for the coordination of neuronal clocks and propose a new cellular target, astrocytes, for neuropharmacology of transient or chronic perturbation of circadian rhythms, where alteration of astrocytic clock genes might contribute to the impairment of the neurobehavioural outputs such as cognition.

Indexed as

AnimalsARNTL Transcription FactorsAstrocytesCircadian ClocksCognitiongamma-Aminobutyric AcidMice, KnockoutMotor ActivityNeuronsSequence DeletionSignal TransductionSuprachiasmatic NucleusARNTL Transcription FactorsBmal1 protein, mousegamma-Aminobutyric Acid

Identifiers

PMID28186121
PMCPMC5309809
OpenAlexW2586303004

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.