ArticleMolecular brain2019
Altered cortical Cytoarchitecture in the Fmr1 knockout mouse.
Article in Molecular brain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- GABAergic neurons exhibit subtype-specific changes in the developing somatosensory cortex of a rat model of Fragile X Syndrome.Frontiers in neuroscience · 2026Article
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Developmental Disturbances in Animal Models of Autism Spectrum Disorder.Developmental neurobiology · 2025Review
- Orchestrating Neural Development Through mRNA Translation Regulation.Journal of neurochemistry · 2025Review
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- 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
- The Role of Nde1 phosphorylation in interkinetic nuclear migration and neural migration during cortical development.Molecular biology of the cell · 2024Article
- Hypnotic treatment improves sleep architecture and EEG disruptions and rescues memory deficits in a mouse model of fragile X syndrome.Cell reports · 2024Article
- Topography and Ensemble Activity in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.eNeuro · 2024Article
- Fragile X cortex is characterized by decreased parvalbumin-expressing interneurons.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Fragile X Syndrome as an interneuronopathy: a lesson for future studies and treatments.Frontiers in neuroscience · 2023Review
- Directly reprogrammed fragile X syndrome dorsal forebrain precursor cells generate cortical neurons exhibiting impaired neuronal maturation.Frontiers in cellular neuroscience · 2023Article
- CRISPR/Cas-Based Approaches to Study Schizophrenia and Other Neurodevelopmental Disorders.International journal of molecular sciences · 2022Review
- Single cell transcriptomics reveals dysregulated cellular and molecular networks in a fragile X syndrome model.PLoS genetics · 2022Article
- Pum2 and TDP-43 refine area-specific cytoarchitecture post-mitotically and modulate translation ofeLife · 2022Article
- The inhibition of NCS-1 binding to Ric8a rescues fragile X syndrome mice model phenotypes.Frontiers in neuroscience · 2022Article
- Altered inflammatory response in FMRP-deficient microglia.iScience · 2021Article
- Article
- Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by silencing of the FMR1 gene and subsequent loss of its protein product, fragile X retardation protein (FMRP). One of the most robust neuropathological findings in post-mortem human FXS and Fmr1 KO mice is the abnormal increase in dendritic spine densities, with the majority of spines showing an elongated immature morphology. However, the exact mechanisms of how FMRP can regulate dendritic spine development are still unclear. Abnormal dendritic spines can result from disturbances of multiple factors during neurodevelopment, such as alterations in neuron numbers, position and glial cells. In this study, we undertook a comprehensive histological analysis of the cerebral cortex in Fmr1 KO mice. They displayed significantly fewer neuron and PV-interneuron numbers, along with altered cortical lamination patterns. In terms of glial cells, Fmr1 KO mice exhibited an increase in Olig2-oligodendrocytes, which corresponded to the abnormally higher myelin expression in the corpus callosum. Iba1-microglia were significantly reduced but GFAP-astrocyte numbers and intensity were elevated. Using primary astrocytes derived from KO mice, we further demonstrated the presence of astrogliosis characterized by an increase in GFAP expression and astrocyte hypertrophy. Our findings provide important information on the cortical architecture of Fmr1 KO mice, and insights towards possible mechanisms associated with FXS.
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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 Socratic graph.