ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Dendritic arborization and spine dynamics are abnormal in the mouse model of MECP2 duplication syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 133 citations in OpenAlex.
- Characterization of Electrophysiological and Transcriptomic Alterations in Patient-Derived Neurons from CHAMP1 Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic analysis reveals synaptic dysregulation and mitochondrial dysfunction in autism spectrum disorder.Brain, behavior, & immunity - health · 2026Article
- Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- SEZ6L2 Loss Disrupts Motor Coordination, Cognitive Function, and Synaptic Connectivity.bioRxiv : the preprint server for biology · 2026Article
- MECP2 Duplication Uncouples Mitochondrial and Purine Metabolism During neuronal maturation.bioRxiv : the preprint server for biology · 2025Article
- miR-199a functions downstream of MeCP2 in neurons ofiScience · 2025Article
- MECP2 Dysfunction in Rett Syndrome: Molecular Mechanisms, Multisystem Pathology, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- NEXMIF overexpression is associated with autism-like behaviors and alterations in dendritic arborization and spine formation in mice.Frontiers in neuroscience · 2025Article
- Reducing Filamin A Restores Cortical Synaptic Connectivity and Early Social Communication Following Cellular Mosaicism in Autism Spectrum Disorder Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Human microglial cells as a therapeutic target in a neurodevelopmental disease model.Stem cell reports · 2024Article
- HeterozygousHeliyon · 2024Article
- Tug-of-Peace: Visual Rivalry and Atypical Visual Motion Processing in MECP2 Duplication Syndrome of Autism.eNeuro · 2024Article
- Disruption of the autism gene and chromatin regulator KDM5A alters hippocampal cell identity.Science advances · 2023Article
- Article
- Oxidized linoleic acid metabolites regulate neuronal morphogenesis in vitro.Neurochemistry international · 2023Article
- Unraveling the mysteries of dendritic spine dynamics: Five key principles shaping memory and cognition.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023Article
- Morphological Features of Human Dendritic Spines.Advances in neurobiology · 2023Review
- Aberrant cortical spine dynamics after concussive injury are reversed by integrated stress response inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Aberrant brain functional and structural developments in MECP2 duplication rats.Neurobiology of disease · 2022Article
- Increased Reliability of Visually-Evoked Activity in Area V1 of the MECP2-Duplication Mouse Model of Autism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
MECP2 duplication syndrome is a childhood neurological disorder characterized by intellectual disability, autism, motor abnormalities, and epilepsy. The disorder is caused by duplications spanning the gene encoding methyl-CpG-binding protein-2 (MeCP2), a protein involved in the modulation of chromatin and gene expression. MeCP2 is thought to play a role in maintaining the structural integrity of neuronal circuits. Loss of MeCP2 function causes Rett syndrome and results in abnormal dendritic spine morphology and decreased pyramidal dendritic arbor complexity and spine density. The consequences of MeCP2 overexpression on dendritic pathophysiology remain unclear. We used in vivo two-photon microscopy to characterize layer 5 pyramidal neuron spine turnover and dendritic arborization as a function of age in transgenic mice expressing the human MECP2 gene at twice the normal levels of MeCP2 (Tg1; Collins et al., 2004). We found that spine density in terminal dendritic branches is initially higher in young Tg1 mice but falls below control levels after postnatal week 12, approximately correlating with the onset of behavioral symptoms. Spontaneous spine turnover rates remain high in older Tg1 animals compared with controls, reflecting the persistence of an immature state. Both spine gain and loss rates are higher, with a net bias in favor of spine elimination. Apical dendritic arbors in both simple- and complex-tufted layer 5 Tg1 pyramidal neurons have more branches of higher order, indicating that MeCP2 overexpression induces dendritic overgrowth. P70S6K was hyperphosphorylated in Tg1 somatosensory cortex, suggesting that elevated mTOR signaling may underlie the observed increase in spine turnover and dendritic growth.
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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.