ArticleNeurobiology of disease2013
Neuronal morphology in MeCP2 mouse models is intrinsically variable and depends on age, cell type, and Mecp2 mutation.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- D-Fructose Exposure Impairs Neuronal Development in Mouse Neural Stem Cells.International journal of molecular sciences · 2026Article
- Editing DNA methylation in vivo.Nature communications · 2025Article
- MeCP2 interacts with the super elongation complex to regulate transcription.Science advances · 2025Article
- Altered dendritic morphology of MEC II pyramidal and stellate cells in Rett syndrome mice.Frontiers in neuroanatomy · 2025Article
- Male autism spectrum disorder is linked to brain aromatase disruption by prenatal BPA in multimodal investigations and 10HDA ameliorates the related mouse phenotype.Nature communications · 2024Article
- Sex- and age-dependent contribution of System xFrontiers in behavioral neuroscience · 2023Article
- Aberrant astrocyte protein secretion contributes to altered neuronal development in multiple models of neurodevelopmental disorders.Nature neuroscience · 2022Article
- A single-cell atlas reveals the heterogeneity of meningeal immunity in a mouse model of Methyl CpG binding protein 2 deficiency.Frontiers in immunology · 2022Article
- Sex disparate gut microbiome and metabolome perturbations precede disease progression in a mouse model of Rett syndrome.Communications biology · 2021Article
- Hyperexcitability and brain morphological differences in mice lacking the cystine/glutamate antiporter, system xJournal of neuroscience research · 2021Article
- Motor training improves coordination and anxiety in symptomaticScience advances · 2021Article
- Perineuronal net degradation rescues CA2 plasticity in a mouse model of Rett syndrome.The Journal of clinical investigation · 2021Article
- The enhancement of activity rescues the establishment of Mecp2 null neuronal phenotypes.EMBO molecular medicine · 2021Article
- Sex differences in Mecp2-mutant Rett syndrome model mice and the impact of cellular mosaicism in phenotype development.Brain research · 2020Review
- MeCP2: A Critical Regulator of Chromatin in Neurodevelopment and Adult Brain Function.International journal of molecular sciences · 2019Review
- Article
- Unique Sensory and Motor Behavior in Thy1-GFP-M Mice before and after Spinal Cord Injury.Journal of neurotrauma · 2018Article
- Autism spectrum disorder: neuropathology and animal models.Acta neuropathologica · 2017Review
- Neuronal cytoskeletal gene dysregulation and mechanical hypersensitivity in a rat model of Rett syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Rett Syndrome (RTT), a progressive neurological disorder characterized by developmental regression and loss of motor and language skills, is caused by mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MECP2). Neurostructural phenotypes including decreased neuronal size, dendritic complexity, and spine density have been reported in postmortem RTT brain tissue and in Mecp2 animal models. How these changes in neuronal morphology are related to RTT-like phenotype and MeCP2 function, and the extent to which restoration of neuronal morphology can be used as a cellular readout in therapeutic studies, however, remain unclear. Here, we systematically examined neuronal morphology in vivo across three Mecp2 mouse models representing Mecp2 loss-of-function, partial loss-of-function, and gain-of-function mutations, at developmental time points corresponding to early- and late-symptomatic RTT-like behavioral phenotypes. We found that in Mecp2 loss-of-function mouse models, dendritic complexity is reduced in a mild, age-dependent, and brain region-specific manner, whereas soma size is reduced consistently throughout development. Neither phenotype, however, is altered in Mecp2 gain-of-function mice. Our results suggest that, in the cell types we examined, the use of dendritic morphology as a cellular readout of RTT phenotype and therapeutic efficacy should be cautioned, as it is intrinsically variable. In contrast, soma size may be a robust and reliable marker for evaluation of MeCP2 function in Mecp2 loss-of-function studies.
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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.