ArticleFrontiers in cellular neuroscience2022
Pharmacological determination of the fractional block of Nav channels required to impair neuronal excitability and
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Seize the Data: A User-Friendly GUI for High-Resolution Analysis of Seizure Dynamics in HD-MEA Recordings.eNeuro · 2026Article
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- The underlying mechanism of scorpion venom peptide BmK AS in reducing epilepsy seizures: mediated through dual modulation of Nav1.6 and the inflammasome pathway.Frontiers in pharmacology · 2026Article
- Enhancing neural signal quality: a spike-denoising model with BiLSTM and attention mechanism.Brain informatics · 2025Article
- Activation of Dopamine D1 Receptors at the Axon Initial Segment-Like Process of Retinal AII Amacrine Cells Modulates Action Potential Firing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Differential roles of NaeLife · 2025Article
- An Open-Source 3D-Printed Recording Stage with Customizable Chambers for Ex Vivo Experiments.eNeuro · 2024Article
- Article
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channels (Nav) are essential for the initiation and propagation of action potentials in neurons. Of the nine human channel subtypes, Nav1.1, Nav1.2 and Nav1.6 are prominently expressed in the adult central nervous system (CNS). All three of these sodium channel subtypes are sensitive to block by the neurotoxin tetrodotoxin (TTX), with TTX being almost equipotent on all three subtypes. In the present study we have used TTX to determine the fractional block of Nav channels required to impair action potential firing in pyramidal neurons and reduce network seizure-like activity. Using automated patch-clamp electrophysiology, we first determined the IC
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