ArticleProceedings of the National Academy of Sciences of the United States of America2016
Jointly reduced inhibition and excitation underlies circuit-wide changes in cortical processing in Rett syndrome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
104 citing papers in PubMed, 183 citations in OpenAlex.
- Trial
- Early differential impact of MeCP2 mutations on functional networks in Rett syndrome patient-derived human cortical organoids.Nature communications · 2026Article
- MeCP2 regulates telencephalic development in human cerebral organoids.Cell reports · 2025Article
- Degraded sensory coding in a mouse model ofbioRxiv : the preprint server for biology · 2025Article
- Altered oscillatory coupling reflects possible inhibitory interneuron dysfunction in Rett syndrome.medRxiv : the preprint server for health sciences · 2025Article
- Article
- Chloride Homeostasis in Neuronal Disorders: Bridging Measurement to Therapy.Life (Basel, Switzerland) · 2025Review
- Learning-Associated Flexibility of Cortical Taste Coding Is Impaired in Shank3 Knockout Mice.bioRxiv : the preprint server for biology · 2025Article
- Article
- A genetically encoded actuator boosts L-type calcium channel function in diverse physiological settings.Science advances · 2024Article
- Degraded tactile coding in the Cntnap2 mouse model of autism.Cell reports · 2024Article
- Heterogeneous subpopulations of GABAiScience · 2024Article
- The selfish network: how the brain preserves behavioral function through shifts in neuronal network state.Trends in neurosciences · 2024Review
- Unraveling the socio-cognitive consequences of KCC2 disruption in zebrafish: implications for neurodevelopmental disorders and therapeutic interventions.Frontiers in molecular neuroscience · 2024Article
- Drug repurposing in Rett and Rett-like syndromes: a promising yet underrated opportunity?Frontiers in medicine · 2024Article
- Neuronal KActa pharmacologica Sinica · 2024Review
- Microcircuit failure in STXBP1 encephalopathy leads to hyperexcitability.Cell reports. Medicine · 2023Article
- Selective Deletion of Methyl CpG Binding Protein 2 from Parvalbumin Interneurons in the Auditory Cortex Delays the Onset of Maternal Retrieval in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Interneuron-Targeted Disruption ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Brain Mitochondrial Bioenergetics in Genetic Neurodevelopmental Disorders: Focus on Down, Rett and Fragile X Syndromes.International journal of molecular sciences · 2023Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Rett syndrome (RTT) arises from loss-of-function mutations in methyl-CpG binding protein 2 gene (Mecp2), but fundamental aspects of its physiological mechanisms are unresolved. Here, by whole-cell recording of synaptic responses in MeCP2 mutant mice in vivo, we show that visually driven excitatory and inhibitory conductances are both reduced in cortical pyramidal neurons. The excitation-to-inhibition (E/I) ratio is increased in amplitude and prolonged in time course. These changes predict circuit-wide reductions in response reliability and selectivity of pyramidal neurons to visual stimuli, as confirmed by two-photon imaging. Targeted recordings reveal that parvalbumin-expressing (PV
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Registered trials
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.