ArticleNeuron2012
NMDA receptor regulation prevents regression of visual cortical function in the absence of Mecp2.
Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
118 citing papers in PubMed, 190 citations in OpenAlex.
- Variability in sensory processing and evoked potentials in Rett syndrome.medRxiv : the preprint server for health sciences · 2026Article
- Suppression of astrocyte BMP signaling improves molecular signatures and functional deficits in a fragile X syndrome mouse model.Nature communications · 2026Article
- Visual Recovery Reflects Cortical MeCP2 Sensitivity in Rett Syndrome.Annals of clinical and translational neurology · 2026Article
- Loss of the Mecp2 gene in parvalbumin interneurons leads to an inhibitory deficit in the amygdala and affects its functional connectivity.Molecular autism · 2026Article
- Novel binding mode for negative allosteric NMDA receptor modulators.The Journal of general physiology · 2026Article
- CDKL5 deficiency results in atypical subregion-specific expression of perineuronal nets during mouse visual critical period.Frontiers in neuroscience · 2026Article
- Mecp2 deficiency impairs microscale cortical network topology and dynamics in a Rett syndrome mouse model.bioRxiv : 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
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- MeCP2 prevents against sustained ketamine-induced synaptic depression at inhibitory synapses.iScience · 2025Article
- fNIRS as a biomarker for X-linked neurodevelopmental disorders: leveraging visual processing to assess brain function?Frontiers in neuroscience · 2025Article
- Multidimensional Analysis of a Social Behavior Identifies Regression and Phenotypic Heterogeneity in a Female Mouse Model for Rett Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Akap5 links synaptic dysfunction to neuroinflammatory signaling in a mouse model of infantile neuronal ceroid lipofuscinosis.Frontiers in synaptic neuroscience · 2024Article
- Wild-type MECP2 expression coincides with age-dependent sensory phenotypes in a female mouse model for Rett syndrome.Journal of neuroscience research · 2023Article
- Rett Syndrome: A Tale of Altered Genetics, Synaptic Plasticity, and Neurodevelopmental Dynamics.Cureus · 2023Review
- A Potential Biomarker of Brain Activity in Autism Spectrum Disorders: A Pilot fNIRS Study in Female Preschoolers.Brain sciences · 2023Article
- A working taxonomy for describing the sensory differences of autism.Molecular autism · 2023Review
- Circuit-level theories for sensory dysfunction in autism: convergence across mouse models.Frontiers in neurology · 2023Review
- Optogenetic stimulation shapes dendritic trees of infragranular cortical pyramidal cells.Frontiers in cellular neuroscience · 2023Article
- A Global Multiregional Proteomic Map of the Human Cerebral Cortex.Genomics, proteomics & bioinformatics · 2022Article
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Brain function is shaped by postnatal experience and vulnerable to disruption of Methyl-CpG-binding protein, Mecp2, in multiple neurodevelopmental disorders. How Mecp2 contributes to the experience-dependent refinement of specific cortical circuits and their impairment remains unknown. We analyzed vision in gene-targeted mice and observed an initial normal development in the absence of Mecp2. Visual acuity then rapidly regressed after postnatal day P35-40 and cortical circuits largely fell silent by P55-60. Enhanced inhibitory gating and an excess of parvalbumin-positive, perisomatic input preceded the loss of vision. Both cortical function and inhibitory hyperconnectivity were strikingly rescued independent of Mecp2 by early sensory deprivation or genetic deletion of the excitatory NMDA receptor subunit, NR2A. Thus, vision is a sensitive biomarker of progressive cortical dysfunction and may guide novel, circuit-based therapies for Mecp2 deficiency.
Indexed as
Identifiers
What OpenQuestion holds
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.