ArticleBrain and behavior2015
Persistent astrocyte activation in the fragile X mouse cerebellum.
Article in Brain and behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- The role of astrocytes in autism spectrum disorder and associated syndromes: Evidence, animal models, mechanisms, and therapeutic potential.Zoological research · 2026Review
- Article
- Neuroimmune mechanisms in autism etiology - untangling a complex problem using human cellular models.Oxford open neuroscience · 2024Article
- Astrocytes in fragile X syndrome.Frontiers in cellular neuroscience · 2023Review
- The Cerebellar Involvement in Autism Spectrum Disorders: From the Social Brain to Mouse Models.International journal of molecular sciences · 2022Review
- Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.Frontiers in synaptic neuroscience · 2022Review
- Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2021Article
- Disrupted Association of Sensory Neurons With Enveloping Satellite Glial Cells in Fragile X Mouse Model.Frontiers in molecular neuroscience · 2021Article
- Rethinking Intellectual Disability from Neuro- to Astro-Pathology.International journal of molecular sciences · 2020Review
- Lipopolysaccharide-induced inflammation leads to acute elevations in pro-inflammatory cytokine expression in a mouse model of Fragile X syndrome.Physiology & behavior · 2020Article
- Altered cortical Cytoarchitecture in the Fmr1 knockout mouse.Molecular brain · 2019Article
- TNF-α increases the intrinsic excitability of cerebellar Purkinje cells through elevating glutamate release in Bergmann Glia.Scientific reports · 2018Article
- Modeling Inflammation in Autism Spectrum Disorders Using Stem Cells.Frontiers in pediatrics · 2018Review
- Regulation of IL-6 Secretion by Astrocytes via TLR4 in the Fragile X Mouse Model.Frontiers in molecular neuroscience · 2018Article
- Astrocytic Contributions to Synaptic and Learning Abnormalities in a Mouse Model of Fragile X Syndrome.Biological psychiatry · 2017Article
- Dysfunctional mTORC1 Signaling: A Convergent Mechanism between Syndromic and Nonsyndromic Forms of Autism Spectrum Disorder?International journal of molecular sciences · 2017Review
- AThe Journal of cell biology · 2017Article
- Imbalance between Glutamate and GABA in Fmr1 Knockout Astrocytes Influences Neuronal Development.Genes · 2016Article
- Denervated hippocampus provides a favorable microenvironment for neuronal differentiation of endogenous neural stem cells.Neural regeneration research · 2016Article
- Persistent astrocyte activation in the fragile X mouse cerebellum.Brain and behavior · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFragile X Syndrome, the most common single gene cause of autism, results from loss of the RNA-binding protein FMRP. Although FMRP is highly expressed in neurons, it has also recently been identified in glia. It has been postulated that in the absence of FMRP, abnormal function of non-neuronal cells may contribute to the pathogenesis of the disorder. We previously demonstrated reduced numbers of oligodendrocyte precursor cells and delayed myelination in the cerebellum of fragile X (Fmr1) knockout mice.
methodsWe used quantitative western blotting and immunocytochemistry to examine the status of astrocytes and microglia in the cerebellum of Fmr1 mice during development and in adulthood.
resultsWe report increased expression of the astrocyte marker GFAP in the cerebellum of Fmr1 mice starting in the second postnatal week and persisting in to adulthood. At 2 weeks postnatal, expression of Tumor Necrosis Factor Receptor 2 (TNFR2) and Leukemia Inhibitory Factor (LIF) were elevated in the Fmr1 KO cerebellum. In adults, expression of TNFR2 and the glial marker S100β were also elevated in Fmr1 knockouts, but LIF expression was not different from wild-type mice. We found no evidence of microglial activation or neuroinflammation at any age examined.
conclusionsThese findings demonstrate an atypical pattern of astrogliosis in the absence of microglial activation in Fmr1 knockout mouse cerebellum. Enhanced TNFR2 and LIF expression in young mice suggests that changes in the expression of astrocytic proteins may be an attempt to compensate for delayed myelination in the developing cerebellum of Fmr1 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.