Evidence map›Paper›PMID 26250775›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

Mutation of the Dyslexia-Associated Gene Dcdc2 Enhances Glutamatergic Synaptic Transmission Between Layer 4 Neurons in Mouse Neocortex.

Alicia Che, Dongnhu T Truong, R Holly Fitch, Joseph J LoTurco

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Animal models of developmental dyslexia.Frontiers in neuroscience · 2022
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Individual Differences in Reading Skill Are Related to Trial-by-Trial Neural Activation Variability in the Reading Network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Article
  10. Article
  11. Neural Noise Hypothesis of Developmental Dyslexia.Trends in cognitive sciences · 2017
    Review
  12. Article
  13. Review
  14. Study of Genetic Association WithClinical practice and epidemiology in mental health : CP & EMH · 2017
    Article
  15. Article
  16. 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

4 authors at 3 institutions in 1 country.

Alicia CheDepartment of Physiology and Neurobiology.
Dongnhu T TruongDepartment of Psychology, University of Connecticut, Storrs, CT 06269, USA.
R Holly FitchDepartment of Psychology, University of Connecticut, Storrs, CT 06269, USA.
Joseph J LoTurcoDepartment of Physiology and Neurobiology.
Cornell University · USUniversity of Connecticut · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
PROJ 3: NEUROBEHAVIOR: BEHAVIOTAL CONSEQUENCES OF EMBRYONIC DISRUPTIONP01HD057853 · NICHD · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GALABURDA, ALBERT MARK · 2009 to 2014
$5.3M
DYSLEXIA SUSCEPTIBILITY GENES AND MECHANISMS OF NEURONAL DEVELOPMENTR01HD055655 · NICHD · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2008 to 2012
$1.6M
NCATS NIH HHS UL1 TR001863NICHD NIH HHS P01 HD057853NICHD NIH HHS R01 HD055655
6 · The paper itself

Abstract

Variants in DCDC2 have been associated with reading disability in humans, and targeted mutation of Dcdc2 in mice causes impairments in both learning and sensory processing. In this study, we sought to determine whether Dcdc2 mutation affects functional synaptic circuitry in neocortex. We found mutation in Dcdc2 resulted in elevated spontaneous and evoked glutamate release from neurons in somatosensory cortex. The probability of release was decreased to wild-type level by acute application of N-methyl-d-aspartate receptor (NMDAR) antagonists when postsynaptic NMDARs were blocked by intracellular MK-801, and could not be explained by elevated ambient glutamate, suggesting altered, nonpostsynaptic NMDAR activation in the mutants. In addition, we determined that the increased excitatory transmission was present at layer 4-layer 4 but not thalamocortical connections in Dcdc2 mutants, and larger evoked synaptic release appeared to enhance the NMDAR-mediated effect. These results demonstrate an NMDAR activation-gated, increased functional excitatory connectivity between layer 4 lateral connections in somatosensory neocortex of the mutants, providing support for potential changes in cortical connectivity and activation resulting from mutation of dyslexia candidate gene Dcdc2.

Indexed as

AnimalsGlutamic AcidMiceMicrotubule-Associated ProteinsMutationNeocortexNerve NetNeuronsNeurotransmitter AgentsSomatosensory CortexSynaptic TransmissionUp-RegulationDCDC2 protein, mouseGlutamic AcidMicrotubule-Associated ProteinsNeurotransmitter Agentsglutamate releaseNMDA receptorpaired recordingpresynapticreading disability

Identifiers

PMID26250775
PMCPMC5004750
OpenAlexW2270777660

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.