Evidence map›Paper›PMID 26683074›Full record

ArticleJournal of neurophysiology2016

Enhancement of postsynaptic GABAA and extrasynaptic NMDA receptor-mediated responses in the barrel cortex of Mecp2-null mice.

Fu-Sun Lo, Mary E Blue, Reha S Erzurumlu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Review
  9. How the Barrel Cortex Became a Working Model for Developmental Plasticity: A Historical Perspective.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  10. Review
  11. Article
  12. Rett Syndrome and CDKL5 Deficiency Disorder: From Bench to Clinic.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Synaptopathology Involved in Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2018
    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

3 authors at 2 institutions in 1 country.

Fu-Sun LoDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland; and.
Mary E BlueHugo W. Moser Research Institute at Kennedy Krieger, Inc. and Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Reha S ErzurumluDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland; and rerzurumlu@som.umaryland.edu.
University of Maryland, Baltimore · USKennedy Krieger Institute · US

Funding

Translational Neuroscience CoreU54HD079123 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI FATEMI, S. ALI · 2014 to 2019
$7.9M
Thalamocortical circuit defects in developmental brain disordersR01NS092216 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI ERZURUMLU, REHA S · 2015 to 2019
$2.9M
NICHD NIH HHS U54 HD-079123NICHD NIH HHS U54 HD079123NINDS NIH HHS NS-092216NINDS NIH HHS R01 NS092216
6 · The paper itself

Abstract

Rett syndrome (RTT) is a neurodevelopmental disorder that results from mutations in the X-linked gene for methyl-CpG-binding protein 2 (MECP2). The underlying cellular mechanism for the sensory deficits in patients with RTT is largely unknown. This study used the Bird mouse model of RTT to investigate sensory thalamocortical synaptic transmission in the barrel cortex of Mecp2-null mice. Electrophysiological results showed an excitation/inhibition imbalance, biased toward inhibition, due to an increase in efficacy of postsynaptic GABAA receptors rather than alterations in inhibitory network and presynaptic release properties. Enhanced inhibition impaired the transmission of tonic sensory signals from the thalamus to the somatosensory cortex. Previous morphological studies showed an upregulation of NMDA receptors in the neocortex of both RTT patients and Mecp2-null mice at early ages [Blue ME, Naidu S, Johnston MV. Ann Neurol 45: 541-545, 1999; Blue ME, Kaufmann WE, Bressler J, Eyring C, O'Driscoll C, Naidu S, Johnston MV. Anat Rec (Hoboken) 294: 1624-1634, 2011]. Although AMPA and NMDA receptor-mediated excitatory synaptic transmission was not altered in the barrel cortex of Mecp2-null mice, extrasynaptic NMDA receptor-mediated responses increased markedly. These responses were blocked by memantine, suggesting that extrasynaptic NMDA receptors play an important role in the pathogenesis of RTT. The results suggest that enhancement of postsynaptic GABAA and extrasynaptic NMDA receptor-mediated responses may underlie impaired somatosensation and that pharmacological blockade of extrasynaptic NMDA receptors may have therapeutic value for RTT.

Indexed as

AnimalsFemaleMaleMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLReceptors, GABA-AReceptors, N-Methyl-D-AspartateRett SyndromeSomatosensory CortexSynapsesSynaptic PotentialsThalamusMecp2 protein, mouseMethyl-CpG-Binding Protein 2Receptors, GABA-AReceptors, N-Methyl-D-Aspartatebarrel cortexexcitation/inhibition balanceMecp2 geneRett syndrome

Identifiers

PMID26683074
PMCPMC4808090
OpenAlexW2208245974

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.