Cited by 201Genetics and Neurodevelopmental DisordersNeuroscience and Neuropharmacology ResearchAutism Spectrum Disorder Research

Circuit and Plasticity Defects in the Developing Somatosensory Cortex of Fmr1 Knock-Out Mice

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Bureau, Ingrid, Shepherd, Gordon M. G., Svoboda, Karel·2008·The Journal of Neuroscience

Abstract

Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 knock-out(ko) mice, the specific cortical circuits affected in the syndrome are unknown. Here, we investigated the development of excitatory projections in the barrel cortex of Fmr1 ko mice. In 2-week-old Fmr1 ko mice, a major ascending projection connecting layer 4 (L4) to L3 (L4→L3), was defective in multiple and independent ways: its strength was reduced, caused by a lower connection probability; the axonal arbors of L4 cells were spatially diffuse in L2/3; the L4→L3 projection did not show experience-dependent plasticity. By 3 weeks, the strength of the L4→L3 projection was similar to that of wild type. Our data indicate that Fmr1 shapes sensory cortical circuits during a developmental critical period.

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Crossref · 10.1523/jneurosci.1076-08.2008

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  • Fmr1 mutant mice have a significant delay in the stabilization of dendritic spines and in the maturation of thalamocortical and corticocortical synapses, defects associated with a temporal shift in the critical period for sensory-induced plasticity across different cortical areas.

    “Fmr1 mutant mice have a significant delay in the stabilization of dendritic spines and in the maturation of thalamocortical and corticocortical synapses 94-98 , defects associated with a temporal shift in the critical period for sensory-induced plasticity across different cortical areas 94,97,99-101 .”

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Authors
Bureau, I., Shepherd, G. M. G., & Svoboda, K.
Affiliations
Howard Hughes Medical Institute (US)
Corresponding author
Bureau, Ingrid
Venue
The Journal of Neuroscience
Published
2008-05-14
Volume
28
Issue
20
Pages
5178-5188
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W1966371094
Cited by
201
References
82
Citations by year
2026: 3 · 2025: 6 · 2024: 8 · 2023: 8 · 2022: 6 · 2021: 14 · 2020: 14 · 2019: 8 · 2018: 8 · 2017: 11 · 2016: 8 · 2015: 13 · 2014: 14 · 2013: 12 · 2012: 17
FWCI
9.69
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
  • HAL (submittedVersion)
Funders
  • Howard Hughes Medical Institute
  • FRAXA Research Foundation
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (R01NS038259)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
Keywords
FMR1 gene, fragile X syndrome, Fmr1 knockout mice, barrel cortex, somatosensory cortex, cortical circuit development, synaptic plasticity, axonal arbors, experience-dependent plasticity, critical period, connection probability
MeSH terms
Animals, Disease Models, Animal, Fragile X Syndrome, Male, Mice, Inbred C57BL, Nervous System Malformations, Neural Pathways, Synaptic Transmission, Neuronal Plasticity, Organ Culture Techniques, Sensation, Somatosensory Cortex, Mice, Knockout, Gene Expression Regulation, Developmental, Excitatory Postsynaptic Potentials, Genetic Predisposition to Disease, Growth Cones, Mice, Fragile X Messenger Ribonucleoprotein 1

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