ArticleMolecular psychiatry2019
Critical period inhibition of NKCC1 rectifies synapse plasticity in the somatosensory cortex and restores adult tactile response maps in fragile X mice.
Article in Molecular psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 74 citations in OpenAlex.
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- Article
- Infant sensory gating and a developmental cascade to autistic traits and anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Molecular psychiatry · 2026Article
- Subtype- and Layer-Specific Developmental Gradients of Postnatal GABAergic Neurons in the Rodent Barrel Cortex.Developmental neuroscience · 2025Article
- Autophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.Research square · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- The NKCC1 Inhibitor Bumetanide Restores Cortical Feedforward Inhibition and Lessens Sensory Hypersensitivity in Early Postnatal Fragile X Mice.Biological psychiatry · 2025Article
- Prepartum bumetanide treatment reverses altered neonatal social communication but nonspecifically reduces postpubertal social behavior in a mouse model of fragile X syndrome.Genomic psychiatry : advancing science from genes to society · 2025Article
- Restoring transient connectivity during development improves dysfunctions in fragile X mice.bioRxiv : the preprint server for biology · 2024Article
- Degraded tactile coding in the Cntnap2 mouse model of autism.Cell reports · 2024Article
- Article
- Delaying the GABA Shift Indirectly Affects Membrane Properties in the Developing Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- High-Sensitivity Intrinsic Optical Signal Imaging Through Flexible, Low-Cost Adaptations of an Upright Microscope.eNeuro · 2023Article
- The TgF344-AD rat: behavioral and proteomic changes associated with aging and protein expression in a transgenic rat model of Alzheimer's disease.Neurobiology of aging · 2023Article
- Review
- Circuit-level theories for sensory dysfunction in autism: convergence across mouse models.Frontiers in neurology · 2023Review
- Neurodevelopment and early pharmacological interventions in Fragile X Syndrome.Frontiers in neuroscience · 2023Review
- From circuits to behavior: Amygdala dysfunction in fragile X syndrome.Frontiers in integrative neuroscience · 2023Review
- R1441C and G2019S LRRK2 knockin mice have distinct striatal molecular, physiological, and behavioral alterations.Communications biology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Sensory perturbations in visual, auditory and tactile perception are core problems in fragile X syndrome (FXS). In the Fmr1 knockout mouse model of FXS, the maturation of synapses and circuits during critical period (CP) development in the somatosensory cortex is delayed, but it is unclear how this contributes to altered tactile sensory processing in the mature CNS. Here we demonstrate that inhibiting the juvenile chloride co-transporter NKCC1, which contributes to altered chloride homeostasis in developing cortical neurons of FXS mice, rectifies the chloride imbalance in layer IV somatosensory cortex neurons and corrects the development of thalamocortical excitatory synapses during the CP. Comparison of protein abundances demonstrated that NKCC1 inhibition during early development caused a broad remodeling of the proteome in the barrel cortex. In addition, the abnormally large size of whisker-evoked cortical maps in adult Fmr1 knockout mice was corrected by rectifying the chloride imbalance during the early CP. These data demonstrate that correcting the disrupted driving force through GABA
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