Evidence map›Paper›PMID 28717969›Full record

ArticleMolecular neurobiology2018

Decreasing the Expression of GABA

Verónica Vidal, Susana García-Cerro, Paula Martínez, Andrea Corrales, Sara Lantigua, Rebeca Vidal, Noemí Rueda, Laurence Ozmen, Maria-Clemencia Hernández, Carmen Martínez-Cué

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. 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 15% 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, 17 citations in OpenAlex.

  1. The role of GABANeuroscience and biobehavioral reviews · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Selective Modulation of α5 GABAFrontiers in cellular neuroscience · 2020
    Article
  10. Enhanced Dendritic Inhibition and Impaired NMDAR Activation in a Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  11. 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

10 authors at 3 institutions in 2 countries.

Verónica VidalDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Susana García-CerroDepartamento de Fundamentos Clínicos, Unidad de Farmacología, Universitat de Barcelona, Barcelona, Spain.
Paula MartínezDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Andrea CorralesDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Sara LantiguaDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Rebeca VidalDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Noemí RuedaDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain.
Laurence OzmenPharma Research and Early Development, Hoffman-La Roche Ltd., Basel, Switzerland.
Maria-Clemencia HernándezPharma Research and Early Development, Hoffman-La Roche Ltd., Basel, Switzerland.
Carmen Martínez-CuéDepartamento de Fisiología y Farmacología, Facultad de Medicina, Universidad deCantabria, Santander, Spain. martinec@unican.es.ORCID http://orcid.org/0000-0002-2137-1156
Universidad de Cantabria · ESRoche (Switzerland) · CHUniversitat de Barcelona · ES

Funding

Ministerio de Economía y Competitividad PSI2016-76194-R/ AEI/FEDER/UE
6 · The paper itself

Abstract

Trisomy 21 or Down syndrome (DS) is the most common cause of intellectual disability of a genetic origin. The Ts65Dn (TS) mouse, which is the most commonly used and best-characterized mouse model of DS, displays many of the cognitive, neuromorphological, and biochemical anomalies that are found in the human condition. One of the mechanisms that have been proposed to be responsible for the cognitive deficits in this mouse model is impaired GABA-mediated inhibition. Because of the well-known modulatory role of GABA

Indexed as

CognitionElectrophysiological PhenomenaAnimalsCell CountCell DifferentiationCell ProliferationCrosses, GeneticDisease Models, AnimalDown SyndromeFemaleGene DosageHippocampusMaleMice, KnockoutNeuronsReceptors, GABA-AGabra5 protein, mouseReceptors, GABA-ACognitionDown syndromeGABAAOverinhibitionTs65Dn miceα5 Subunit

Identifiers

PMID28717969
OpenAlexW2735179394

What OpenQuestion holds

Textmetadata
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.