ArticleCell reports2016
Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
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- Altered ECM deposition and cell adhesion signaling in a human cortical organoid model of fragile X syndrome.Molecular brain · 2026Article
- Fmr1 knockout disrupts multiple intrinsic properties via reduced HCN channel activity in mediodorsal thalamocortical neurons.Experimental physiology · 2026Article
- CA2 neurons show abnormal responses to social stimuli in a rat model of Fragile X syndrome.bioRxiv : the preprint server for biology · 2025Article
- Early onset of hyperexcitability of medial mammillary body neurons in 5XFADJournal of neurophysiology · 2025Article
- ErbB inhibition rescues nigral dopamine neuron hyperactivity and repetitive behaviors in a mouse model of fragile X syndrome.Molecular psychiatry · 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
- FMRP Controls Neuronal Architecture and Synaptic Content of NMDA Receptors in Cultured Hippocampal Neurons.Journal of molecular neuroscience : MN · 2025Article
- Anterior piriform cortex dysfunction underlies autism spectrum disorders-related olfactory deficits in Fmr1 conditional deletion mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Age-related increase in the excitability of mouse layer V pyramidal neurons in the primary motor cortex is accompanied by an increased persistent inward current.GeroScience · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Elevated somatostatin interneuron long-term potentiation minimally regulates temporoammonic plasticity in a mouse model of Fragile X Syndrome.Frontiers in pharmacology · 2025Article
- Conotoxin KM-RIIIJ reveals interplay between KScientific reports · 2024Article
- Exosomal TNF-α mediates voltage-gated Na+ channel 1.6 overexpression and contributes to brain tumor-induced neuronal hyperexcitability.The Journal of clinical investigation · 2024Article
- Altered brain serotonin 5-HTNeuropharmacology · 2024Article
- Circuit-based intervention corrects excessive dentate gyrus output in the fragile X mouse model.eLife · 2024Article
- Hyperexcitability in the Olfactory Bulb and Impaired Fine Odor Discrimination in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Circuit-based intervention corrects excessive dentate gyrus output in the Fragile X mouse model.bioRxiv : the preprint server for biology · 2023Article
- Rescue of sharp wave-ripples and prevention of network hyperexcitability in the ventral but not the dorsal hippocampus of a rat model of fragile X syndrome.Frontiers in cellular neuroscience · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Altered neuronal excitability is one of the hallmarks of fragile X syndrome (FXS), but the mechanisms underlying this critical neuronal dysfunction are poorly understood. Here, we find that pyramidal cells in the entorhinal cortex of Fmr1 KO mice, an established FXS mouse model, display a decreased AP threshold and increased neuronal excitability. The AP threshold changes in Fmr1 KO mice are caused by increased persistent sodium current (INaP). Our results indicate that this abnormal INaP in Fmr1 KO animals is mediated by increased mGluR5-PLC-PKC (metabotropic glutamate receptor 5/phospholipase C/protein kinase C) signaling. These findings identify Na(+) channel dysregulation as a major cause of neuronal hyperexcitability in cortical FXS neurons and uncover a mechanism by which abnormal mGluR5 signaling causes neuronal hyperexcitability in a FXS mouse model.
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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.