ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Fast-onset long-term open-state block of sodium channels by A-type FHFs mediates classical spike accommodation in hippocampal pyramidal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 63 citations in OpenAlex.
- Article
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- Long-term inactivation mediated by different FGF-A homologues on heterologously expressed NaV1.2 currents.The Journal of general physiology · 2026Article
- Missense Variants in the A Isoform of FGF13 as a Novel Cause of Paroxysmal Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Effects of open-channel blocking peptides in NaBiophysical journal · 2025Article
- Loss of intracellular FGF14 (iFGF14) increases excitability of mature hippocampal pyramidal neurons.The Journal of general physiology · 2025Article
- Article
- Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism.eLife · 2025Article
- Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism.bioRxiv : the preprint server for biology · 2024Article
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- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Long-Term Inactivation of Sodium Channels as a Mechanism of Adaptation in CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels.eLife · 2022Article
- Article
- Article
- Slow recovery from fast inactivation of Nav1.3 channels: a common gating mechanism shared in sweet- and sour-sensing cells.Pflugers Archiv : European journal of physiology · 2021Article
- Slow recovery from the inactivation of voltage-gated sodium channel Nav1.3 in mouse taste receptor cells.Pflugers Archiv : European journal of physiology · 2021Article
- Fast inactivation of Nav1.3 channels by FGF14 proteins: An unconventional way to regulate the slow firing of adrenal chromaffin cells.The Journal of general physiology · 2021Article
- Fast inactivation of Nav current in rat adrenal chromaffin cells involves two independent inactivation pathways.The Journal of general physiology · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Classical accommodation is a form of spike frequency adaptation in neurons whereby excitatory drive results in action potential output of gradually decreasing frequency. Here we describe an essential molecular component underlying classical accommodation in juvenile mouse hippocampal CA1 pyramidal neurons. A-type isoforms of fibroblast growth factor homologous factors (FHFs) bound to axosomatic voltage-gated sodium channels bear an N-terminal blocking particle that drives some associated channels into a fast-onset, long-term inactivated state. Use-dependent accumulating channel blockade progressively elevates spike voltage threshold and lengthens interspike intervals. The FHF particle only blocks sodium channels from the open state, and mutagenesis studies demonstrate that this particle uses multiple aliphatic and cationic residues to both induce and maintain the long-term inactivated state. The broad expression of A-type FHFs in neurons throughout the vertebrate CNS suggests a widespread role of these sodium channel modulators in the control of neural firing.
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