Evidence map›Paper›PMID 29358017›Full record

ArticleNeuron2018

Normal CA1 Place Fields but Discoordinated Network Discharge in a Fmr1-Null Mouse Model of Fragile X Syndrome.

Zoe Nicole Talbot, Fraser Todd Sparks, Dino Dvorak, Bridget Mary Curran, Juan Marcos Alarcon, André Antonio Fenton

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 82 citations in OpenAlex.

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  11. Hippocampal Place Cell Sequences Are Impaired in a Rat Model of Fragile X Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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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 3 institutions in 1 country.

Zoe Nicole TalbotSchool of Medicine, New York University, New York, NY 10016, USA.
Fraser Todd SparksCenter for Neural Science, New York University, New York, NY 10003, USA.
Dino DvorakCenter for Neural Science, New York University, New York, NY 10003, USA.
Bridget Mary CurranDepartment of Pathology, Robert F. Furchgott Center for Neuroscience, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA.
Juan Marcos AlarconDepartment of Pathology, Robert F. Furchgott Center for Neuroscience, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA.
André Antonio FentonCenter for Neural Science, New York University, New York, NY 10003, USA; Neuroscience Institute at the New York University Langone Medical Center, New York, NY 10016, USA; Department of Physiology & Pharmacology, Robert F. Furchgott Center for Neuroscience, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA. Electronic address: afenton@nyu.edu.
New York University · USState University of New York · USSUNY Downstate Health Sciences University · US

Funding

Training Program in NeuroscienceT32MH096331 · NIMH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KLANN, ERIC, RUDY, BERNARDO · 2011 to 2019
$2.6M
Translation, Synchrony, and CognitionR01MH099128 · NIMH · NEW YORK UNIVERSITY · PI FENTON, ANDRE ANTONIO · 2013 to 2017
$2.0M
Neural coordination and discoordination in Fmr1 null miceR01NS105472 · NINDS · NEW YORK UNIVERSITY · PI FENTON, ANDRE ANTONIO · 2017 to 2021
$1.8M
Experience-dependent Modulation of Synaptic Circuits in the HippocampusR21NS091830 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI ALARCON, JUAN MARCOS · 2015 to 2016
$456k
NIMH NIH HHS R01 MH099128NIMH NIH HHS T32 MH096331NINDS NIH HHS R01 NS105472NINDS NIH HHS R21 NS091830
6 · The paper itself

Abstract

Silence of FMR1 causes loss of fragile X mental retardation protein (FMRP) and dysregulated translation at synapses, resulting in the intellectual disability and autistic symptoms of fragile X syndrome (FXS). Synaptic dysfunction hypotheses for how intellectual disabilities like cognitive inflexibility arise in FXS predict impaired neural coding in the absence of FMRP. We tested the prediction by comparing hippocampus place cells in wild-type and FXS-model mice. Experience-driven CA1 synaptic function and synaptic plasticity changes are excessive in Fmr1-null mice, but CA1 place fields are normal. However, Fmr1-null discharge relationships to local field potential oscillations are abnormally weak, stereotyped, and homogeneous; also, discharge coordination within Fmr1-null place cell networks is weaker and less reliable than wild-type. Rather than disruption of single-cell neural codes, these findings point to invariant tuning of single-cell responses and inadequate discharge coordination within neural ensembles as a pathophysiological basis of cognitive inflexibility in FXS. VIDEO ABSTRACT.

Indexed as

Long-Term PotentiationAnimalsAvoidance LearningCA1 Region, HippocampalDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeLearningMaleMice, Inbred C57BLMice, KnockoutPlace CellsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1autismFmr1FMRPfragile X syndromeintellectual disabilitylearningmemoryneural coordinationplace cellsynaptic plasticity

Identifiers

PMID29358017
PMCPMC6066593
OpenAlexW2668834229

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.