Evidence map›Paper›PMID 28213518›Full record

ArticleThe Journal of biological chemistry2017

Deficits in the activity of presynaptic γ-aminobutyric acid type B receptors contribute to altered neuronal excitability in fragile X syndrome.

Ji-Yong Kang, Jayashree Chadchankar, Thuy N Vien, Michelle I Mighdoll, Thomas M Hyde, Robert J Mather, Tarek Z Deeb, Menelas N Pangalos, Nicholas J Brandon, John Dunlop and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
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  13. Review
  14. Keeping the Balance: GABABrain sciences · 2022
    Review
  15. CaInternational journal of molecular sciences · 2022
    Review
  16. GABACurrent topics in behavioral neurosciences · 2022
    Review
  17. Presynaptic GABAPflugers Archiv : European journal of physiology · 2021
    Article
  18. Article
  19. Neurexins regulate presynaptic GABANature communications · 2021
    Article
  20. Review
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

11 authors at 5 institutions in 2 countries.

Ji-Yong KangFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Jayashree ChadchankarFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Thuy N VienFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Michelle I Mighdollthe Lieber Institute for Brain Development and.
Thomas M Hydethe Lieber Institute for Brain Development and.
Robert J MatherFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Tarek Z DeebFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Menelas N PangalosInnovative Medicines and Early Development, AstraZeneca, Melbourn Science Park, Cambridge Road, Royston Herts SG8 6EE, United Kingdom, and.
Nicholas J BrandonFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
John DunlopFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111.
Stephen J MossFrom the AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111, Stephen.Moss@Tufts.edu.
AstraZeneca (United States) · USJohns Hopkins University · USLieber Institute for Brain Development · USMelbourn Science Park · GBTufts University · US

Funding

Constructing inhibitory synapsesR01NS051195 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI MOSS, STEPHEN J · 2006 to 2014
$3.2M
Modulation of KCC2 activity and the postnatal development of synaptic inhibitionR01NS101888 · NINDS · TUFTS UNIVERSITY BOSTON · PI DEEB, TAREK ZIAD, MOSS, STEPHEN J · 2017 to 2021
$2.3M
Dissecting Mechanisms of GABAB-GIRK Plasticity with PsychostimulantsR01DA037170 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MOSS, STEPHEN J, SLESINGER, PAUL A · 2014 to 2018
$2.1M
Novel actions of neurosteroids on GABA (A) receptor traffickingR01MH097446 · NIMH · TUFTS UNIVERSITY BOSTON · PI DAVIES, PAUL ANDREW, MOSS, STEPHEN J · 2013 to 2017
$2.1M
Deficits in KCC2 activity and the pathophysiology of Status EpilepticusR01NS087662 · NINDS · TUFTS UNIVERSITY BOSTON · PI MOSS, STEPHEN J · 2014 to 2018
$2.0M
The role of ubiquitination in regulating GABA(A) receptor functional expressionR01NS056359 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI MOSS, STEPHEN J · 2007 to 2010
$1.4M
Deficits in KCC2 activity and the pathophysiology of Autism spectrum disordersR21MH106954 · NIMH · TUFTS UNIVERSITY BOSTON · PI MOSS, STEPHEN J · 2015 to 2016
$454k
Impaired KCC2 function underlies pharmacoresistant seizuresR21NS080064 · NINDS · TUFTS UNIVERSITY BOSTON · PI MOSS, STEPHEN J · 2013 to 2014
$452k
NIDA NIH HHS R01 DA037170NIMH NIH HHS R01 MH097446NIMH NIH HHS R21 MH106954NINDS NIH HHS R01 NS051195NINDS NIH HHS R01 NS056359NINDS NIH HHS R01 NS087662NINDS NIH HHS R01 NS101888NINDS NIH HHS R21 NS080064
6 · The paper itself

Abstract

The behavioral and anatomical deficits seen in fragile X syndrome (FXS) are widely believed to result from imbalances in the relative strengths of excitatory and inhibitory neurotransmission. Although modified neuronal excitability is thought to be of significance, the contribution that alterations in GABAergic inhibition play in the pathophysiology of FXS are ill defined. Slow sustained neuronal inhibition is mediated by γ-aminobutyric acid type B (GABA

Indexed as

AgedAged, 80 and overAnimalsBehavior, AnimalDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1Fragile X Syndromegamma-Aminobutyric AcidGlutamic AcidHippocampusHumansMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1gamma-Aminobutyric AcidGlutamic AcidReceptors, GABA-BRNA, MessengerSerinefragile XGABA receptorinhibition mechanismneurotransmitter receptorpresynapticsynapseγ-aminobutyric acid (GABA)

Identifiers

PMID28213518
PMCPMC5399111
OpenAlexW2588115154

What Socratic 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 Socratic graph.