ArticleBiological psychiatry2017
Astrocytic Contributions to Synaptic and Learning Abnormalities in a Mouse Model of Fragile X Syndrome.
Article in Biological psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 82 citations in OpenAlex.
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- The role of astrocytes in autism spectrum disorder and associated syndromes: Evidence, animal models, mechanisms, and therapeutic potential.Zoological research · 2026Review
- Dissociating the Hallucinogenic and Neuroplastic Effects of Psilocybin.bioRxiv : the preprint server for biology · 2026Article
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- Contribution of astrocytic calcium signaling to auditory hypersensitivity in a mouse model of fragile X syndrome.Neurobiology of disease · 2026Article
- Astrocytic GABA controls fidelity of temporal cortical processing in Fragile X Syndrome.Neurobiology of disease · 2026Article
- Activity of Human-Specific Interlaminar Astrocytes in a Chimeric Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2025Article
- Activity of human-specific Interlaminar Astrocytes in a Chimeric Mouse Model of Fragile X Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Astrocyte-neuron crosstalk in neurodevelopmental disorders.Current opinion in neurobiology · 2024Review
- Purinergic Signalling Mediates Aberrant Excitability of Developing Neuronal Circuits in the Fmr1 Knockout Mouse Model.Molecular neurobiology · 2024Article
- Dysregulated Purinergic Signalling in Fragile X Syndrome Cortical Astrocytes.Neuromolecular medicine · 2024Article
- The role of glia in the dysregulation of neuronal spinogenesis in Ube3a-dependent ASD.Experimental neurology · 2024Article
- The intersection of sleep and synaptic translation in synaptic plasticity deficits in neurodevelopmental disorders.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Review
- Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model.Nature communications · 2024Article
- Translational modulator ISRIB alleviates synaptic and behavioral phenotypes in Fragile X syndrome.iScience · 2024Article
- Article
- Development of anFrontiers in pharmacology · 2024Article
- Rare genetic brain disorders with overlapping neurological and psychiatric phenotypes.Nature reviews. Neurology · 2024Review
- Prenatal folic acid and vitamin BCommunications biology · 2023Article
- Altered Purinergic Signaling in Neurodevelopmental Disorders: Focus on P2 Receptors.Biomolecules · 2023Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundFragile X syndrome (FXS) is the most common type of mental retardation attributable to a single-gene mutation. It is caused by FMR1 gene silencing and the consequent loss of its protein product, fragile X mental retardation protein. Fmr1 global knockout (KO) mice recapitulate many behavioral and synaptic phenotypes associated with FXS. Abundant evidence suggests that astrocytes are important contributors to neurological diseases. This study investigates astrocytic contributions to the progression of synaptic abnormalities and learning impairments associated with FXS.
methodsTaking advantage of the Cre-lox system, we generated and characterized mice in which fragile X mental retardation protein is selectively deleted or exclusively expressed in astrocytes. We performed in vivo two-photon imaging to track spine dynamics/morphology along dendrites of neurons in the motor cortex and examined associated behavioral defects.
resultsWe found that adult astrocyte-specific Fmr1 KO mice displayed increased spine density in the motor cortex and impaired motor-skill learning. The learning defect coincided with a lack of enhanced spine dynamics in the motor cortex that normally occurs in response to motor skill acquisition. Although spine density was normal at 1 month of age in astrocyte-specific Fmr1 KO mice, new spines formed at an elevated rate. Furthermore, fragile X mental retardation protein expression in only astrocytes was insufficient to rescue most spine or behavioral defects.
conclusionsOur work suggests a joint astrocytic-neuronal contribution to FXS pathogenesis and reveals that heightened spine formation during adolescence precedes the overabundance of spines and behavioral defects found in adult Fmr1 KO mice.
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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 OpenQuestion graph.