ArticleFrontiers in physiology2022
Cinacalcet inhibition of neuronal action potentials preferentially targets the fast inactivated state of voltage-gated sodium channels.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Divalent cation depletion enhances intrinsic neuronal excitability through CaSR-dependent modulation of threshold ion channels.PNAS nexus · 2026Article
- Exploring multiple drug actions of a CaNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- Neurovirulent cytokines increase neuronal excitability in a model of coronavirus-induced neuroinflammation.Intensive care medicine experimental · 2023Article
- Somatic and terminal CB1 receptors are differentially coupled to voltage-gated sodium channels in neocortical neurons.Cell reports · 2023Article
- PLC regulates spontaneous glutamate release triggered by extracellular calcium and readily releasable pool size in neocortical neurons.Frontiers in cellular neuroscience · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-gated sodium channel (VGSC) activation is essential for action potential generation in the brain. Allosteric calcium-sensing receptor (CaSR) agonist, cinacalcet, strongly and ubiquitously inhibits VGSC currents in neocortical neurons
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Registered trials
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