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Cited by 252Genetics and Neurodevelopmental DisordersNeuroscience and Neuropharmacology ResearchAutism Spectrum Disorder Research

Critical period plasticity is disrupted in the barrel cortex of FMR1 knockout mice

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Harlow, Emily G., Till, Sally M., Russell, Theron A., Wijetunge, Lasani S., Kind, Peter, Contractor, Anis·2010·Neuron
DOI 10.1016/j.neuron.2010.01.024PMC PMC2825250
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Abstract

Alterations in sensory processing constitute prominent symptoms of fragile X syndrome; however, little is known about how disrupted synaptic and circuit development in sensory cortex contributes to these deficits. To investigate how the loss of fragile X mental retardation protein (FMRP) impacts the development of cortical synapses, we examined excitatory thalamocortical synapses in somatosensory cortex during the perinatal critical period in Fmr1 knockout mice. FMRP ablation resulted in dysregulation of glutamatergic signaling maturation. The fraction of silent synapses persisting to later developmental times was increased; there was a temporal delay in the window for synaptic plasticity, while other forms of developmental plasticity were not altered in Fmr1 knockout mice. Our results indicate that FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts the timing of the critical period for layer IV synaptic plasticity.

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Crossref · 10.1016/j.neuron.2010.01.024

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  • FMRP is required for normal developmental progression of synaptic maturation, and loss of this RNA binding protein impacts synaptic plasticity in late embryonic stages and during the first postnatal days.

    “Specifically, FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts on synaptic plasticity in late embryonic stages and during the first postnatal days (Harlow et al. 2010).”

    From Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories (2018) · cites this paper as Harlow et al. 2010

  • In Fmr1 knockout mice, activity-dependent maturation of excitatory thalamocortical synapses is dysregulated, causing persistence of silent NMDA-receptor-only synapses at times when they would normally express both NMDA and AMPA receptors.

    “In Fmr1 knockout mice, this activity-dependent maturation of the excitatory thalamocortical synapses is dysregulated, resulting in a persistence of silent NMDA-receptor-only synapses at times during brain development when these synapses would normally express both NMDA and AMPA receptors63.”

    From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [63]

  • The absence of AMPA receptors at these synapses may be due in part to dysregulation of Arc mRNA translation in Fmr1 knockout mice.

    “The absence of AMPA receptors at these synapses may be due, in part, to the dysregulation of Arc mRNA translation that occurs in Fmr1 knockout mice.”

    From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [63]

  • 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 .”

    From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [97]

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Authors
Harlow, E. G., Till, S. M., Russell, T. A., Wijetunge, L. S., Kind, P., & Contractor, A.
Affiliations
  • Northwestern University (US)
  • University of Edinburgh (GB)
Corresponding author
Contractor, Anis
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2010-02
Volume
65
Issue
3
Pages
385-398
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2010.01.024
PMC
PMC2825250
OpenAlex
W2151856267
Cited by
252
References
71
Citations by year
2026: 5 · 2025: 8 · 2024: 20 · 2023: 11 · 2022: 12 · 2021: 17 · 2020: 19 · 2019: 15 · 2018: 16 · 2017: 15 · 2016: 18 · 2015: 16 · 2014: 20 · 2013: 17 · 2012: 16
FWCI
10.80
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
Funders
  • Autism Speaks (AS1348)
  • FRAXA Research Foundation
  • Brain Research Foundation
  • National Institutes of Health
  • National Institute of Mental Health (T32MH067564)
  • National Institute of Neurological Disorders and Stroke (R01NS058894)
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
fragile X syndrome, FMRP, Fmr1 knockout mice, critical period, barrel cortex, somatosensory cortex, thalamocortical synapses, synaptic plasticity, silent synapses, glutamatergic signaling, synapse maturation, RNA-binding proteins, layer 4
MeSH terms
Disks Large Homolog 4 Protein, Age Factors, Animals, Animals, Newborn, Electric Stimulation, Membrane Proteins, Mice, Inbred C57BL, Neural Pathways, Neuronal Plasticity, Somatosensory Cortex, Thalamus, Time Factors, Vibrissae, 2-Amino-5-phosphonovalerate, Microscopy, Immunoelectron, Receptors, Glutamate, Long-Term Potentiation, Mice, Knockout, Patch-Clamp Techniques, Gene Expression Regulation, Developmental, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, Intracellular Signaling Peptides and Proteins, Mice, Guanylate Kinases, Fragile X Mental Retardation Protein, Fragile X Messenger Ribonucleoprotein 1, In Vitro Techniques

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