ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Fragile X mental retardation protein is required for rapid experience-dependent regulation of the potassium channel Kv3.1b.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Intellectual Disability and Potassium Channelopathies: A Systematic Review.Frontiers in genetics · 2020Pooled it
- Electroretinography biomarkers indicate disrupted visual processing in Fragile X syndrome.Journal of neurodevelopmental disorders · 2026Article
- FMRP restoration in parvalbumin interneurons: A circuit-specific improvement of visual learning in fragile X syndrome.iScience · 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
- Sex-specific loss of mitochondrial membrane integrity in the auditory brainstem of a mouse model of Fragile X Syndrome.Open biology · 2025Article
- Topography and Ensemble Activity in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.eNeuro · 2024Article
- Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model.Nature communications · 2024Article
- Voltage-gated potassium channels as a potential therapeutic target for the treatment of neurological and psychiatric disorders.Frontiers in cellular neuroscience · 2024Review
- Modulation of potassium conductances optimizes fidelity of auditory information.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Peripheral Fragile X messenger ribonucleoprotein is required for the timely closure of a critical period for neuronal susceptibility in the ventral cochlear nucleus.Frontiers in cellular neuroscience · 2023Article
- Tonotopic differentiation of presynaptic neurotransmitter-releasing machinery in the auditory brainstem during the prehearing period and its selective deficits in Fmr1 knockout mice.The Journal of comparative neurology · 2022Article
- A sound-driven cortical phase-locking change in the Fmr1 KO mouse requires Fmr1 deletion in a subpopulation of brainstem neurons.Neurobiology of disease · 2022Article
- Mechanisms Driving the Emergence of Neuronal Hyperexcitability in Fragile X Syndrome.International journal of molecular sciences · 2022Review
- The role of altered translation in intellectual disability and epilepsy.Progress in neurobiology · 2022Review
- Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022Review
- Bumetanide for Irritability in Children With Sensory Processing Problems Across Neurodevelopmental Disorders: A Pilot Randomized Controlled Trial.Frontiers in psychiatry · 2022Article
- Absence of the Fragile X messenger ribonucleoprotein alters response patterns to sounds in the auditory midbrain.Frontiers in neuroscience · 2022Article
- Auditory Dysfunction in Animal Models of Autism Spectrum Disorder.Frontiers in molecular neuroscience · 2022Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Fragile X mental retardation protein (FMRP) is an RNA-binding protein that regulates synaptic plasticity by repressing translation of specific mRNAs. We found that FMRP binds mRNA encoding the voltage-gated potassium channel Kv3.1b in brainstem synaptosomes. To explore the regulation of Kv3.1b by FMRP, we investigated Kv3.1b immunoreactivity and potassium currents in the auditory brainstem sound localization circuit of male mice. The unique features of this circuit allowed us to control neuronal activity in vivo by exposing animals to high-frequency, amplitude-modulated stimuli, which elicit predictable and stereotyped patterns of input to the anterior ventral cochlear nucleus (AVCN) and medial nucleus of the trapezoid body (MNTB). In wild-type (WT) animals, Kv3.1b is expressed along a tonotopic gradient in the MNTB, with highest levels in neurons at the medial, high-frequency end. At baseline, Fmr1(-/-) mice, which lack FMRP, displayed dramatically flattened tonotopicity in Kv3.1b immunoreactivity and K(+) currents relative to WT controls. Moreover, after 30 min of acoustic stimulation, levels of Kv3.1b immunoreactivity were significantly elevated in both the MNTB and AVCN of WT, but not Fmr1(-/-), mice. These results suggest that FMRP is necessary for maintenance of the gradient in Kv3.1b protein levels across the tonotopic axis of the MNTB, and are consistent with a role for FMRP as a repressor of protein translation. Using numerical simulations, we demonstrate that Kv3.1b tonotopicity may be required for accurate encoding of stimulus features such as modulation rate, and that disruption of this gradient, as occurs in Fmr1(-/-) animals, degrades processing of this information.
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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.