ArticleNature neuroscience2014
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1(-/y) mice.
Article in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.
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Who cites it
144 citing papers in PubMed.
- SPG601-associated modulation of resting-state EEG and improvement in executive function in a fragile X syndrome randomized controlled crossover study.Scientific reports · 2026Trial
- Dysregulated GluA2-Y876 phosphorylation contributes to loss of synaptic upscaling in GRIP1 mutant mice with reduced sociability and increased repetitive behavior.Molecular psychiatry · 2026Article
- Contribution of astrocytic calcium signaling to auditory hypersensitivity in a mouse model of fragile X syndrome.Neurobiology of disease · 2026Article
- Diminished Signal-to-Noise Ratio Disrupts Somatosensory Population Encoding and Drives Tactile Hyposensitivity in the Fmr1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Enhanced CB1 receptor function in GABAergic neurons mediates hyperexcitability and impaired sensory-driven synchrony of cortical circuits in Fragile X Syndrome model mice.Molecular psychiatry · 2026Article
- A human electrophysiological signature of Fragile X pathophysiology is shared in V1 of Fmr1Nature communications · 2026Article
- Astrocytic GABA controls fidelity of temporal cortical processing in Fragile X Syndrome.Neurobiology of disease · 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
- Early intrinsic excitability plasticity of neocortical engram neurons defines memory formation and precision.Nature communications · 2025Article
- Dysregulated cortical excitability and tau phosphorylation in a β3 integrin mouse model of autism.Brain : a journal of neurology · 2025Article
- Cortical layer-specific abnormalities in auditory responses in a mouse model of Fragile X Syndrome.Neurobiology of disease · 2025Article
- Higher hyperpolarization-activated current in a subpopulation of interneurons in stratum oriens of area CA1 in the hippocampus of fragile X mice.Journal of neurophysiology · 2025Article
- Olfactory dysfunction and altered cortical excitability in the mouse model of Fragile X Syndrome.Biological research · 2025Article
- Convergent depression of activity-dependent bulk endocytosis in rodent models of autism spectrum disorder.Molecular autism · 2025Article
- Impairment in the homeostatic recruitment of layer 5/6 neurons following whisker stimulation in Fmr1 KO mice.Neurobiology of disease · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Delayed structural maturation of inner hair cell ribbon synapses in a mouse model of fragile X syndrome.Frontiers in molecular neuroscience · 2025Article
- Peripheral contributions to resting state brain dynamics.Nature communications · 2024Article
84 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypersensitivity in response to sensory stimuli and neocortical hyperexcitability are prominent features of Fragile X Syndrome (FXS) and autism spectrum disorders, but little is known about the dendritic mechanisms underlying these phenomena. We found that the primary somatosensory neocortex (S1) was hyperexcited in response to tactile sensory stimulation in Fmr1(-/y) mice. This correlated with neuronal and dendritic hyperexcitability of S1 pyramidal neurons, which affect all major aspects of neuronal computation, from the integration of synaptic input to the generation of action potential output. Using dendritic electrophysiological recordings, calcium imaging, pharmacology, biochemistry and a computer model, we found that this defect was, at least in part, attributable to the reduction and dysfunction of dendritic h- and BKCa channels. We pharmacologically rescued several core hyperexcitability phenomena by targeting BKCa channels. Our results provide strong evidence pointing to the utility of BKCa channel openers for the treatment of the sensory hypersensitivity aspects of FXS.
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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.