ArticleCell reports2018
Strong G-Protein-Mediated Inhibition of Sodium Channels.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 17 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
- Melatonin Upregulates Sodium Channel Nav1.5 in Cultured Neonatal Rat Cardiomyocytes.Physiological research · 2025Article
- Resting motor threshold in navigated transcranial magnetic stimulation: relationship between inter-individual variance and distinct clinical and anatomical factors.Acta neurochirurgica · 2025Article
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- High calcium concentrations reduce cellular excitability of mouse MNTB neurons.Brain research · 2023Article
- Neurovirulent cytokines increase neuronal excitability in a model of coronavirus-induced neuroinflammation.Intensive care medicine experimental · 2023Article
- Shared Mechanisms of GABAergic and Opioidergic Transmission Regulate Corticolimbic Reward Systems and Cognitive Aspects of Motivational Behaviors.Brain sciences · 2023Review
- Somatic and terminal CB1 receptors are differentially coupled to voltage-gated sodium channels in neocortical neurons.Cell reports · 2023Article
- Cinacalcet inhibition of neuronal action potentials preferentially targets the fast inactivated state of voltage-gated sodium channels.Frontiers in physiology · 2022Article
- Article
- Neuronal mechanisms underlying opioid-induced respiratory depression: our current understanding.Journal of neurophysiology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated sodium channels (VGSCs) are strategically positioned to mediate neuronal plasticity because of their influence on action potential waveform. VGSC function may be strongly inhibited by local anesthetic and antiepileptic drugs and modestly modulated via second messenger pathways. Here, we report that the allosteric modulators of the calcium-sensing receptor (CaSR) cinacalcet, calindol, calhex, and NPS 2143 completely inhibit VGSC current in the vast majority of cultured mouse neocortical neurons. This form of VGSC current block persisted in CaSR-deficient neurons, indicating a CaSR-independent mechanism. Cinacalcet-mediated blockade of VGSCs was prevented by the guanosine diphosphate (GDP) analog GDPβs, indicating that G-proteins mediated this effect. Cinacalcet inhibited VGSCs by increasing channel inactivation, and block was reversed by prolonged hyperpolarization. Strong cinacalcet inhibition of VGSC currents was also present in acutely isolated mouse cortical neurons. These data identify a dynamic signaling pathway by which G-proteins regulate VGSC current to indirectly modulate central neuronal excitability.
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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.