Delayed Stabilization of Dendritic Spines in Fragile X Mice
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Fragile X syndrome (FXS) causes mental impairment and autism through transcriptional silencing of the Fmr1 gene, resulting in the loss of the RNA-binding protein fragile X mental retardation protein (FMRP). Cortical pyramidal neurons in affected individuals and Fmr1 knock-out (KO) mice have an increased density of dendritic spines. The mutant mice also show defects in synaptic and experience-dependent circuit plasticity, which are known to be mediated in part by dendritic spine dynamics. We used in vivo time-lapse imaging with two-photon microscopy through cranial windows in male and female neonatal mice to test the hypothesis that dynamics of dendritic protrusions are altered in KO mice during early postnatal development. We find that layer 2/3 neurons from wild-type mice exhibit a rapid decrease in dendritic spine dynamics during the first 2 postnatal weeks, as immature filopodia are replaced by mushroom spines. In contrast, KO mice show a developmental delay in the downregulation of spine turnover and in the transition from immature to mature spine subtypes. Blockade of metabotropic glutamate receptor (mGluR) signaling, which reverses some adult phenotypes of KO mice, accentuated this immature protrusion phenotype in KO mice. Thus, absence of FMRP delays spine stabilization and dysregulated mGluR signaling in FXS may partially normalize this early synaptic defect.
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In our xenotransplantation assay, human cortical neurons show increasingly stable dendritic spine dynamics, comparable to juvenile mouse cortical neurons.
“These experiments revealed that in our xenotransplantation assay, human cortical neurons show increasingly stable dendritic spine dynamics, comparable to juvenile mouse cortical neurons”
From Xenotransplanted human cortical neurons reveal species-specific development and functional integration into mouse visual circuits (2019) · cites this paper as Cruz-Martín et al., 2010
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 [95]
Fmr1 knockout mice show delayed spine maturation.
“They also show a delayed maturation of spines [75]”
From Experience-dependent structural plasticity in the cortex (2011) · cites this paper as [75]
Both recent studies found a significant increase in spine turnover in the barrel cortex of Fmr1 knockout mice.
“Both studies reveal a significant increase in spine turnover in the barrel cortex of Fmr1 KO mice.”
From Experience-dependent structural plasticity in the cortex (2011) · cites this paper as [75]
Spines on apical dendrites of layer 2/3 pyramidal neurons in rodent barrel cortex exhibit gradually decreasing motility and turnover rate between postnatal day 7 and 24.
“For example, spines on the apical dendrites of layer 2/3 pyramidal neurons in rodent barrel cortex exhibit gradually decreasing motility (elongation and shortening of spines) and turnover rate (defined as the total amount of gains and losses of spines) between postnatal day 7 and 24 (P7-24; Lendvai et al., 2000; Cruz-Martin et al., 2010).”
From Spatiotemporal dynamics of dendritic spines in the living brain (2014) · cites this paper as Cruz-Martin et al., 2010
Spine density continuously increases over P7-24 in rodent barrel cortex.
“Nevertheless, spine density continuously increases over this period of time (Cruz-Martin et al., 2010).”
From Spatiotemporal dynamics of dendritic spines in the living brain (2014) · cites this paper as Cruz-Martin et al., 2010
In Fragile X syndrome model animals, spine turnover increased in various cortical areas.
“In vivo studies further showed that in such animals spine turnover increased in various cortical areas (Cruz-Martin et al., 2010; Pan et al., 2010; Padmashri et al., 2013), and neither whisker trimming nor motor learning could further alter spine dynamics (Pan et al., 2010; Padmashri et al., 2013).”
From Spatiotemporal dynamics of dendritic spines in the living brain (2014) · cites this paper as Cruz-Martin et al., 2010
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- Authors
- Cruz-Martin, A., Crespo, M., & Portera-Cailliau, C.
- Affiliations
- Pediatrics and Genetics (US)
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-06-09
- Volume
- 30
- Issue
- 23
- Pages
- 7793-7803
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2903441
- OpenAlex
- W2012010559
- Cited by
- 321
- References
- 80
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 14 · 2023: 15 · 2022: 18 · 2021: 24 · 2020: 25 · 2019: 19 · 2018: 18 · 2017: 24 · 2016: 27 · 2015: 23 · 2014: 34 · 2013: 28 · 2012: 16
- FWCI
- 12.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- FRAXA Research Foundation
- National Institutes of Health
- National Institute of General Medical Sciences
- National Institute of Child Health and Human Development
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD054453)
- 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, spine dynamics, filopodia, mushroom spines, layer 2/3 pyramidal neurons, synaptic plasticity
- MeSH terms
- Animals, Animals, Newborn, Disease Models, Animal, Fragile X Syndrome, Male, Mice, Inbred C57BL, Pseudopodia, Pyridines, Receptors, Metabotropic Glutamate, Mice, Knockout, Excitatory Amino Acid Antagonists, Dendritic Spines, Mice, Fragile X Messenger Ribonucleoprotein 1, Fragile X Mental Retardation Protein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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