Evidence map›Paper›PMID 27939580›Full record

ArticleNeuron2016

MicroRNA-101 Regulates Multiple Developmental Programs to Constrain Excitation in Adult Neural Networks.

Giordano Lippi, Catarina C Fernandes, Laura A Ewell, Danielle John, Benedetto Romoli, Giulia Curia, Seth R Taylor, E Paxon Frady, Anne B Jensen, Jerry C Liu and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. Small Differences and Big Changes: The Many Variables of MicroRNA Expression and Function in the Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Therapeutic Implications of microRNAs in Depressive Disorders: A Review.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
  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

18 authors at 2 institutions in 2 countries.

Giordano LippiDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: glippi@ucsd.edu.
Catarina C FernandesDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Laura A EwellDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Danielle JohnDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Benedetto RomoliDepartment of Biomedical, Metabolic, and Neural Sciences, Center for Neuroscience and Neurotechnology, University of Modena and Reggio Emilia, Modena 41125, Italy.
Giulia CuriaDepartment of Biomedical, Metabolic, and Neural Sciences, Center for Neuroscience and Neurotechnology, University of Modena and Reggio Emilia, Modena 41125, Italy.
Seth R TaylorDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
E Paxon FradyDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Anne B JensenDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Jerry C LiuDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Melanie M ChaabaneDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Cherine BelalDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Jason L NathansonInstitute for Genomic Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Michele ZoliDepartment of Biomedical, Metabolic, and Neural Sciences, Center for Neuroscience and Neurotechnology, University of Modena and Reggio Emilia, Modena 41125, Italy.
Jill K LeutgebDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA; Center for Neural Circuits and Behavior, University of California, San Diego, La Jolla, CA 92093, USA.
Giuseppe BiaginiDepartment of Biomedical, Metabolic, and Neural Sciences, Center for Neuroscience and Neurotechnology, University of Modena and Reggio Emilia, Modena 41125, Italy.
Gene W YeoInstitute for Genomic Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Darwin K BergDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: dberg@ucsd.edu.
University of California San Diego · USUniversity of Modena and Reggio Emilia · IT

Funding

Signal Transduction at Neuronal Nicotinic SynapsesR01NS012601 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1985 to 2016
$5.3M
MicroRNA101 and the Termination of Early Phase Neural DevelopmentR21NS087342 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 2014 to 2015
$426k
Long-Lasting Changes in Neural Networks Induced by Early Exposure to NicotineR21DA038296 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 2015 to 2016
$424k
NIDA NIH HHS R21 DA038296NINDS NIH HHS R01 NS012601NINDS NIH HHS R21 NS087342
6 · The paper itself

Abstract

A critical feature of neural networks is that they balance excitation and inhibition to prevent pathological dysfunction. How this is achieved is largely unknown, although deficits in the balance contribute to many neurological disorders. We show here that a microRNA (miR-101) is a key orchestrator of this essential feature, shaping the developing network to constrain excitation in the adult. Transient early blockade of miR-101 induces long-lasting hyper-excitability and persistent memory deficits. Using target site blockers in vivo, we identify multiple developmental programs regulated in parallel by miR-101 to achieve balanced networks. Repression of one target, NKCC1, initiates the switch in γ-aminobutyric acid (GABA) signaling, limits early spontaneous activity, and constrains dendritic growth. Kif1a and Ank2 are targeted to prevent excessive synapse formation. Simultaneous de-repression of these three targets completely phenocopies major dysfunctions produced by miR-101 blockade. Our results provide new mechanistic insight into brain development and suggest novel candidates for therapeutic intervention.

Indexed as

AnimalsAnkyrinsBehavior, AnimalBrainDendritesgamma-Aminobutyric AcidGene Expression Regulation, DevelopmentalKinesinsMiceMicroRNAsNerve NetNeural PathwaysPatch-Clamp TechniquesPolymerase Chain ReactionSequence Analysis, RNASolute Carrier Family 12, Member 2Ank2 protein, mouseAnkyrinsgamma-Aminobutyric AcidKif1a protein, mouseKinesinsMicroRNAsMIRN101 microRNA, mouseSlc12a2 protein, mouseSolute Carrier Family 12, Member 2excitation/inhibition (E/I)GABA switchhyper-excitabilitymicroRNAmiR-101network developmentneurodevelopmental disordersNKCC1synaptogenesistarget-site blockers

Identifiers

PMID27939580
PMCPMC5182124
OpenAlexW2560740462

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.