ArticleNeuron2023
Improvement of sensory deficits in fragile X mice by increasing cortical interneuron activity after the critical period.
Article in Neuron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Neonatal expression of human FMRP isoform corrects cortical deficits and improves behavior in a mouse model of fragile X syndrome.Molecular therapy. Nucleic acids · 2026Article
- Optimization of Pyrazole-Based Activators of Kv3.1.ACS medicinal chemistry letters · 2026Article
- Contribution of astrocytic calcium signaling to auditory hypersensitivity in a mouse model of fragile X syndrome.Neurobiology of disease · 2026Article
- Article
- Article
- A human electrophysiological signature of Fragile X pathophysiology is shared in V1 of Fmr1Nature communications · 2026Article
- Combined use of Bumetanide and MGE cell transplantation alleviates neuropathic pain and its mechanism after spinal cord injury in mice.Frontiers in immunology · 2026Article
- Infant sensory gating and a developmental cascade to autistic traits and anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- GABAergic neurons exhibit subtype-specific changes in the developing somatosensory cortex of a rat model of Fragile X Syndrome.Frontiers in neuroscience · 2026Article
- Dysfunctional neural dynamics associated with sensory phenotypes in Fragile X syndrome: insights from mouse models.Journal of neurodevelopmental disorders · 2025Review
- FMRP restoration in parvalbumin interneurons: A circuit-specific improvement of visual learning in fragile X syndrome.iScience · 2025Article
- Degraded sensory coding in a mouse model ofbioRxiv : the preprint server for biology · 2025Article
- Crosstalk Between Astrocytes and Inhibitory Neurons During Maturation: Emerging Mechanisms and Functional Implications.Journal of neurochemistry · 2025Review
- Article
- Loss of FMRP in microglia promotes degeneration of parvalbumin neurons and audiogenic seizures via progranulin insufficiency.bioRxiv : the preprint server for biology · 2025Article
- Interneuron Diversity: How Form Becomes Function.Cold Spring Harbor perspectives in biology · 2025Review
- Dynamic recruitment of PV interneurons in the somatosensory cortex induced by experience dependent plasticity.bioRxiv : the preprint server for biology · 2025Article
- Perinatal serotonin signalling dynamically influences the development of cortical GABAergic circuits with consequences for lifelong sensory encoding.Nature communications · 2025Article
- Disruptions in primary visual cortex physiology and function in a mouse model of Timothy syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Changes in the function of inhibitory interneurons (INs) during cortical development could contribute to the pathophysiology of neurodevelopmental disorders. Using all-optical in vivo approaches, we find that parvalbumin (PV) INs and their immature precursors are hypoactive and transiently decoupled from excitatory neurons in postnatal mouse somatosensory cortex (S1) of Fmr1 KO mice, a model of fragile X syndrome (FXS). This leads to a loss of parvalbumin INs (PV-INs) in both mice and humans with FXS. Increasing the activity of future PV-INs in neonatal Fmr1 KO mice restores PV-IN density and ameliorates transcriptional dysregulation in S1, but not circuit dysfunction. Critically, administering an allosteric modulator of Kv3.1 channels after the S1 critical period does rescue circuit dynamics and tactile defensiveness. Symptoms in FXS and related disorders could be mitigated by targeting PV-INs.
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.