ArticleBiological psychiatry2016
Cell-Specific Regulation of N-Methyl-D-Aspartate Receptor Maturation by Mecp2 in Cortical Circuits.
Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Novel binding mode for negative allosteric NMDA receptor modulators.The Journal of general physiology · 2026Article
- Mecp2 deficiency impairs microscale cortical network topology and dynamics in a Rett syndrome mouse model.bioRxiv : the preprint server for biology · 2025Article
- Intravenous esketamine in pediatric Rett syndrome: An open-label, early phase 1 pilot study.Molecular therapy. Methods & clinical development · 2025Article
- Rett Syndrome: A Tale of Altered Genetics, Synaptic Plasticity, and Neurodevelopmental Dynamics.Cureus · 2023Review
- scHumanNet: a single-cell network analysis platform for the study of cell-type specificity of disease genes.Nucleic acids research · 2023Article
- Aberrant maturation and connectivity of prefrontal cortex in schizophrenia-contribution of NMDA receptor development and hypofunction.Molecular psychiatry · 2022Review
- Excitation and Inhibition Imbalance in Rett Syndrome.Frontiers in neuroscience · 2022Review
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Sensitive period for rescuing parvalbumin interneurons connectivity and social behavior deficits caused by TSC1 loss.Nature communications · 2021Article
- The emerging role of chromatin remodelers in neurodevelopmental disorders: a developmental perspective.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- Drug Studies on Rett Syndrome: From Bench to Bedside.Journal of autism and developmental disorders · 2020Review
- Accelerated Hyper-Maturation of Parvalbumin Circuits in the Absence of MeCP2.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- A Composite Sketch of Fast-Spiking Parvalbumin-Positive Neurons.Cerebral cortex communications · 2020Article
- Altered trajectories of neurodevelopment and behavior in mouse models of Rett syndrome.Neurobiology of learning and memory · 2019Review
- Neuronal network dysfunction in a model for Kleefstra syndrome mediated by enhanced NMDAR signaling.Nature communications · 2019Article
- Rett Syndrome and CDKL5 Deficiency Disorder: From Bench to Clinic.International journal of molecular sciences · 2019Review
- Excitation-inhibition balance as a framework for investigating mechanisms in neuropsychiatric disorders.Molecular psychiatry · 2019Review
- Intellectual and developmental disabilities research centers: Fifty years of scientific accomplishments.Annals of neurology · 2019Review
- NMDA 2A receptors in parvalbumin cells mediate sex-specific rapid ketamine response on cortical activity.Molecular psychiatry · 2019Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEarly postnatal experience shapes N-methyl-D-aspartate receptor (NMDAR) subunit composition and kinetics at excitatory synapses onto pyramidal cells; however, little is known about NMDAR maturation onto inhibitory interneurons.
methodsWe combined whole-cell patch clamp recordings (n = 440) of NMDAR-mediated currents from layer-4-to-layer-2/3 synapses onto pyramidal and green fluorescent protein labeled parvalbumin-positive (PV) interneurons in visual cortex at three developmental ages (15, 30, and 45 postnatal days) with array tomography three-dimensional reconstructions of NMDAR subunits GluN2A- and GluN2B-positive synapses onto PV cells.
resultsWe show that the trajectory of the NMDAR subunit switch is slower in PV interneurons than in excitatory pyramidal cells in visual cortex. Notably, this differential time course is reversed in the absence of methyl-CpG-binding protein, MECP2, the molecular basis for cognitive decline in Rett syndrome and some cases of autism. Additional genetic reduction of GluN2A subunits, which prevents regression of vision in Mecp2-knockout mice, specifically rescues the accelerated NMDAR maturation in PV cells.
conclusionsWe demonstrate 1) the time course of NMDAR maturation is cell-type specific, and 2) a new cell-type specific role for Mecp2 in the development of NMDAR subunit composition. Reducing GluN2A expression in Mecp2-knockout mice, which prevents the decline in visual cortical function, also prevents the premature NMDAR maturation in PV cells. Thus, circuit-based therapies targeting NMDAR subunit composition on PV cells may provide novel treatments for Rett syndrome.
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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.