Evidence map›Paper›PMID 25662825›Full record

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

Mechanisms of Functional Hypoconnectivity in the Medial Prefrontal Cortex of Mecp2 Null Mice.

Michael P Sceniak, Min Lang, Addison C Enomoto, C James Howell, Douglas J Hermes, David M Katz

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Leptin antagonism improves Rett syndrome phenotype in symptomatic Mecp2-deficient mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Article
  3. The CaInternational journal of molecular sciences · 2025
    Review
  4. Prefrontal cortical circuits in social behaviors: an overview.Journal of Zhejiang University. Science. B · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. RIPK1 activation in Mecp2-deficient microglia promotes inflammation and glutamate release in RTT.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Article
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  18. Article
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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

6 authors at 2 institutions in 1 country.

Michael P SceniakDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Min LangDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Addison C EnomotoDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
C James HowellDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Douglas J HermesDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
David M KatzDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Case Western Reserve University · USUniversity School · US

Funding

Respiratory Circuit Dysfunction in Rett SyndromeR01NS057398 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI KATZ, DAVID M. · 2007 to 2013
$3.1M
NINDS NIH HHS R01 NS057398
6 · The paper itself

Abstract

Frontal cortical dysfunction is thought to contribute to cognitive and behavioral features of autism spectrum disorders; however, underlying mechanisms are poorly understood. The present study sought to define how loss of Mecp2, the gene mutated in Rett syndrome (RTT), disrupts function in the murine medial prefrontal cortex (mPFC) using acute brain slices and behavioral testing. Compared with wildtype, pyramidal neurons in the Mecp2 null mPFC exhibit significant reductions in excitatory postsynaptic currents, the duration of excitatory UP-states, evoked population activity, and the ratio of NMDA:AMPA currents, as well as an increase in the relative fraction of NR2B currents. These functional changes are associated with reductions in the density of excitatory dendritic spines, the ratio of vesicular glutamate to GABA transporters and GluN1 expression. In contrast to recent reports on circuit defects in other brain regions, we observed no effect of Mecp2 loss on inhibitory synaptic currents or expression of the inhibitory marker parvalbumin. Consistent with mPFC hypofunction, Mecp2 nulls exhibit respiratory dysregulation in response to behavioral arousal. Our data highlight functional hypoconnectivity in the mPFC as a potential substrate for behavioral disruption in RTT and other disorders associated with reduced expression of Mecp2 in frontal cortical regions.

Indexed as

Membrane PotentialsAction PotentialsAnimalsCalcium SignalingDendritic SpinesElectric StimulationExcitatory Postsynaptic PotentialsInhibitory Postsynaptic PotentialsMethyl-CpG-Binding Protein 2MiceMice, KnockoutNerve Tissue ProteinsNeuronsPrefrontal CortexReceptors, AMPAReceptors, N-Methyl-D-AspartateGprin1 protein, mouseMecp2 protein, mouseMethyl-CpG-Binding Protein 2Nerve Tissue ProteinsReceptors, AMPAReceptors, N-Methyl-D-AspartateVesicular Inhibitory Amino Acid Transport ProteinsViaat protein, mouseAMPAE/I balanceEPSCFluo-4 AMGABAIPSCMeCP2medial prefrontal cortexNMDARett syndromesynaptic

Identifiers

PMID25662825
PMCPMC5006177
OpenAlexW2156145718

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.