ArticleGlia2018
Alterations in CA1 hippocampal synapses in a mouse model of fragile X syndrome.
Article in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Prevalence and practices of immunofluorescent cell image processing: a systematic review.Frontiers in cellular neuroscience · 2023Pooled it
- CB1 receptor inhibition restores synaptoneurosomal alternative splicing landscape in fragile X syndrome mice.iScience · 2026Article
- FMRP Regulates NrCAM Expression via β-catenin and Modulates PSD95, Dendritic Spines and Autism-like Behaviors.Neuroscience bulletin · 2026Article
- Sexual dimorphism of autism-like phenotypes in microglial eIF4E overexpression mice.bioRxiv : the preprint server for biology · 2026Article
- Mll5 haploinsufficiency attenuates microglial phagocytosis through dysregulated TREM2-SGK3-GSK3β signaling and recapitulates ASD-like behaviors in mice.Nature communications · 2026Article
- Age-Related Decline in Dendritic Architecture of Hippocampal CA1 Principal Neurons in a Mouse Model of Fragile X Syndrome.Developmental neurobiology · 2026Article
- Auditory Stimulation Rescues Cognitive Deficit inBrain sciences · 2026Article
- Stimulation of the medial septum diagonal band of broca rescues learning and memory deficits iniScience · 2026Article
- Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Article
- Imaging brain development in a KCNQ2-developmental and epileptic encephalopathy mouse model: identifying early biomarkers for functional and structural brain changes.EBioMedicine · 2025Article
- Impaired synaptosome phagocytosis in macrophages of individuals with autism spectrum disorder.Molecular psychiatry · 2025Article
- FMRP Controls Neuronal Architecture and Synaptic Content of NMDA Receptors in Cultured Hippocampal Neurons.Journal of molecular neuroscience : MN · 2025Article
- Postnatal downregulation of Fmr1 in microglia promotes microglial reactivity and causes behavioural alterations in female mice.Molecular autism · 2025Article
- Alterations of synaptic plasticity in Angelman syndrome model mice are rescued by 5-HT7R stimulation.Progress in neurobiology · 2024Article
- Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism.Journal of neuroinflammation · 2024Article
- Microglial over-pruning of synapses during development in autism-associated SCN2A-deficient mice and human cerebral organoids.Molecular psychiatry · 2024Article
- Bone marrow-derived myeloid cells transiently colonize the brain during postnatal development and interact with glutamatergic synapses.iScience · 2024Article
- KAT6A deficiency impairs cognitive functions through suppressing RSPO2/Wnt signaling in hippocampal CA3.Science advances · 2024Article
- Lifelong absence of microglia alters hippocampal glutamatergic networks but not synapse and spine density.EMBO reports · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X Syndrome (FXS) is the major cause of inherited mental retardation and the leading genetic cause of Autism spectrum disorders. FXS is caused by mutations in the Fragile X Mental Retardation 1 (Fmr1) gene, which results in transcriptional silencing of Fragile X Mental Retardation Protein (FMRP). To elucidate cellular mechanisms involved in the pathogenesis of FXS, we compared dendritic spines in the hippocampal CA1 region of adult wild-type (WT) and Fmr1 knockout (Fmr1-KO) mice. Using diolistic labeling, confocal microscopy, and three-dimensional electron microscopy, we show a significant increase in the diameter of secondary dendrites, an increase in dendritic spine density, and a decrease in mature dendritic spines in adult Fmr1-KO mice. While WT and Fmr1-KO mice had the same mean density of spines, the variance in spine density was three times greater in Fmr1-KO mice. Reduced astrocyte participation in the tripartite synapse and less mature post-synaptic densities were also found in Fmr1-KO mice. We investigated whether the increase in synaptic spine density was associated with altered synaptic pruning during development. Our data are consistent with reduced microglia-mediated synaptic pruning in the CA1 region of Fmr1-KO hippocampi when compared with WT littermates at postnatal day 21, which is the peak period of synaptic pruning in the mouse hippocampus. Collectively, these results support abnormal synaptogenesis and synaptic remodeling in mice deficient in FMRP. Deficits in the maturation and distribution of synaptic spines on dendrites of CA1 hippocampal neurons may play a role in the intellectual disabilities associated with FXS.
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Registered trials
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.