Evidence map›Paper›PMID 24753442›Full record

ArticleHippocampus2014

N-cadherin regulates molecular organization of excitatory and inhibitory synaptic circuits in adult hippocampus in vivo.

Jessica S Nikitczuk, Shekhar B Patil, Bridget A Matikainen-Ankney, Joseph Scarpa, Matthew L Shapiro, Deanna L Benson, George W Huntley

Abstract read
In one paragraph

Article in Hippocampus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  10. Urokinase-Type Plasminogen Activator Protects Cerebral Cortical Neurons from Soluble Aβ-Induced Synaptic Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  11. Article
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  14. Article
  15. Excitatory Synaptic Drive and Feedforward Inhibition in the Hippocampal CA3 Circuit Are Regulated by SynCAM 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Altered Development of Synapse Structure and Function in Striatum Caused by Parkinson's Disease-Linked LRRK2-G2019S Mutation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Activity dependent CAM cleavage and neurotransmission.Frontiers in cellular neuroscience · 2015
    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

7 authors at 2 institutions in 1 country.

Jessica S NikitczukFishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Shekhar B PatilFishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Bridget A Matikainen-AnkneyFishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Joseph ScarpaFishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Matthew L ShapiroFishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Deanna L Benson *Fishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
George W Huntley *Fishberg Department of Neuroscience, Friedman Brain Institute and The Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029.
Icahn School of Medicine at Mount Sinai · USThe Graduate Center, CUNY · US

Funding

SYNAPSE TARGETING AND ASSEMBLYR01NS037731 · NINDS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BENSON, DEANNA L · 1999 to 2010
$2.7M
Role of matrix metalloproteinases in synaptic plasticityR01MH075783 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HUNTLEY, GEORGE W. · 2007 to 2011
$1.8M
Mechanisms of Axon Outgrowth and TargetingR01NS050634 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BENSON, DEANNA L · 2007 to 2010
$1.5M
Temporal requirements for N-cadherin in maintaining stability of synapsesF30MH088058 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI NIKITCZUK, JESSICA · 2009 to 2012
$171k
NIMH NIH HHS F30 MH088058NIMH NIH HHS F30MH088058NIMH NIH HHS MH075783NIMH NIH HHS R01 MH075783NINDS NIH HHS NS037731NINDS NIH HHS NS050634NINDS NIH HHS R01 NS037731NINDS NIH HHS R01 NS050634
6 · The paper itself

Abstract

N-Cadherin and β-catenin form a transsynaptic adhesion complex required for spine and synapse development. In adulthood, N-cadherin mediates persistent synaptic plasticity, but whether the role of N-cadherin at mature synapses is similar to that at developing synapses is unclear. To address this, we conditionally ablated N-cadherin from excitatory forebrain synapses in mice starting in late postnatal life and examined hippocampal structure and function in adulthood. In the absence of N-cadherin, β-catenin levels were reduced, but numbers of excitatory synapses were unchanged, and there was no impact on number or shape of dendrites or spines. However, the composition of synaptic molecules was altered. Levels of GluA1 and its scaffolding protein PSD95 were diminished and the density of immunolabeled puncta was decreased, without effects on other glutamate receptors and their scaffolding proteins. Additionally, loss of N-cadherin at excitatory synapses triggered increases in the density of markers for inhibitory synapses and decreased severity of hippocampal seizures. Finally, adult mutant mice were profoundly impaired in hippocampal-dependent memory for spatial episodes. These results demonstrate a novel function for the N-cadherin/β-catenin complex in regulating ionotropic receptor composition of excitatory synapses, an appropriate balance of excitatory and inhibitory synaptic proteins and the maintenance of neural circuitry necessary to generate flexible yet persistent cognitive and synaptic function.

Indexed as

Animalsbeta CateninCadherinsDendritesDendritic SpinesDisks Large Homolog 4 ProteinGuanylate KinasesHippocampusKainic AcidMaleMembrane ProteinsMemory DisordersMice, Inbred C57BLMice, KnockoutNeural InhibitionNeuronsbeta CateninCadherinsCdh2 protein, mouseCTNNB1 protein, mouseDisks Large Homolog 4 ProteinDlg4 protein, mouseGuanylate KinasesKainic AcidMembrane ProteinsReceptors, AMPAcateninscell adhesion moleculesseizurestransgenicwater maze

Identifiers

PMID24753442
PMCPMC4906961
OpenAlexW2105878002

What OpenQuestion holds

Textmetadata
LicenceTDM
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.