ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Abnormal development of dendritic spines in FMR1 knock-out mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
236 citing papers in PubMed, 1 synthesis or guideline pooled it, 520 citations in OpenAlex.
- Connecting DCX, COMT and FMR1 in social behavior and cognitive impairment.Behavioral and brain functions : BBF · 2022Pooled it
- Altered striatal long-term potentiation in the eIF4E-TG mouse model of autism spectrum disorder.iScience · 2026Article
- Human-specific SRGAP2 paralogs synchronize neotenic microglial maturation and synaptic development.Neuron · 2026Article
- LAMP2A-dependent chaperone mediated autophagy regulates Notch signaling and controls neural stem cell differentiation.Cellular and molecular life sciences : CMLS · 2026Article
- Age-Related Decline in Dendritic Architecture of Hippocampal CA1 Principal Neurons in a Mouse Model of Fragile X Syndrome.Developmental neurobiology · 2026Article
- Dysfunctional synaptic competition at dendritic spines in Fragile X syndrome.bioRxiv : the preprint server for biology · 2026Article
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Molecular psychiatry · 2026Article
- Intact spatial learning in Fmr1Frontiers in behavioral neuroscience · 2026Article
- Disrupted theta synchronization and synaptic connectivity in the visual cortex of Fmr1 KO mice.Nature communications · 2025Article
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Research square · 2025Article
- Anterior piriform cortex dysfunction underlies autism spectrum disorders-related olfactory deficits in Fmr1 conditional deletion mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Autistic behavior is a common outcome of biallelic disruption of PDZD8 in humans and mice.Molecular autism · 2025Article
- Behavioral benefits of GSK-3β inhibition and state-dependent microtubule signatures in theFrontiers in neuroscience · 2025Article
- Deep functional measurements of Fragile X syndrome human neurons reveal multiparametric electrophysiological disease phenotype.Communications biology · 2024Article
- Region-Related Differences in Short-Term Synaptic Plasticity and Synaptotagmin-7 in the Male and Female Hippocampus of a Rat Model of Fragile X Syndrome.International journal of molecular sciences · 2024Article
- Topography and Ensemble Activity in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.eNeuro · 2024Article
- Translational modulator ISRIB alleviates synaptic and behavioral phenotypes in Fragile X syndrome.iScience · 2024Article
- HeterozygousHeliyon · 2024Article
- Growth-suppressor microRNAs mediate synaptic overgrowth and behavioral deficits in Fragile X mental retardation protein deficiency.iScience · 2024Article
- Synaptic cell adhesion molecules contribute to the pathogenesis and progression of fragile X syndrome.Frontiers in cellular neuroscience · 2024Review
176 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X syndrome is caused by a mutation in the FMR1 gene leading to absence of the fragile X mental retardation protein (FMRP). Reports that patients and adult FMR1 knock-out mice have abnormally long dendritic spines of increased density suggested that the disorder might involve abnormal spine development. Because spine length, density, and motility change dramatically in the first postnatal weeks, we analyzed these properties in mutant mice and littermate controls at 1, 2, and 4 weeks of age. To label neurons, a viral vector carrying the enhanced green fluorescent protein gene was injected into the barrel cortex. Layer V neurons were imaged on a two-photon laser scanning microscope in fixed tissue sections. Analysis of >16,000 spines showed clear developmental patterns. Between 1 and 4 weeks of age, spine density increased 2.5-fold, and mean spine length decreased by 17% in normal animals. Early during cortical synaptogenesis, pyramidal cells in mutant mice had longer spines than controls. At 1 week, spine length was 28% greater in mutants than in controls. At 2 weeks, this difference was 10%, and at 4 weeks only 3%. Similarly, spine density was 33% greater in mutants than in controls at 1 week of age. At 2 or 4 weeks of age, differences were not detectable. The spine abnormality was not detected in neocortical organotypic cultures. The transient nature of the spine abnormality in the intact animal suggests that FMRP might play a role in the normal process of dendritic spine growth in coordination with the experience-dependent development of cortical circuits.
Indexed as
Identifiers
11438589PMC6762842W2104921672What OpenQuestion holds
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.