ArticleeLife2021
Enhanced excitability of cortical neurons in low-divalent solutions is primarily mediated by altered voltage-dependence of voltage-gated sodium channels.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Divalent cation depletion enhances intrinsic neuronal excitability through CaSR-dependent modulation of threshold ion channels.PNAS nexus · 2026Article
- Synaptic Facilitation Enhances the Reliability and Precision of High-Frequency Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Evidence Based on Sleep Disorder Exacerbating Postoperative Pain via Kynureninase.Drug design, development and therapy · 2026Article
- Plasma sodium levels are related to resting motor threshold in healthy humans.Scientific reports · 2025Article
- Article
- The role of spontaneous and evoked neuronal activity in protection from impending ischemic stroke during the hyperacute state.Scientific reports · 2025Article
- Unreliable homeostatic action potential broadening in cultured dissociated neurons.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat.Journal of neurochemistry · 2025Article
- Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024Article
- Integrated network pharmacology and phosphoproteomic analyses of Baichanting in Parkinson's disease model mice.Heliyon · 2024Article
- Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current.BMC pharmacology & toxicology · 2024Article
- 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
- Contributions of the Sodium Leak Channel NALCN to Pacemaking of Medial Ventral Tegmental Area and Substantia Nigra Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Somatic and terminal CB1 receptors are differentially coupled to voltage-gated sodium channels in neocortical neurons.Cell reports · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Inhibition of Voltage-Gated NaInternational journal of molecular sciences · 2023Article
- Spike desensitisation as a mechanism for high-contrast selectivity in retinal ganglion cells.Frontiers in cellular neuroscience · 2023Article
- The calcium-sensing receptor (CaSR) regulates zebrafish sensorimotor decision making via a genetically defined cluster of hindbrain neurons.Cell reports · 2022Article
- Effective Perturbations by Small-Molecule Modulators on Voltage-Dependent Hysteresis of Transmembrane Ionic Currents.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Increasing extracellular [Ca2+] ([Ca2+]o) strongly decreases intrinsic excitability in neurons but the mechanism is unclear. By one hypothesis, [Ca2+]o screens surface charge, reducing voltage-gated sodium channel (VGSC) activation and by another [Ca2+]o activates Calcium-sensing receptor (CaSR) closing the sodium-leak channel (NALCN). Here we report that neocortical neurons from CaSR-deficient (Casr-/-) mice had more negative resting potentials and did not fire spontaneously in reduced divalent-containing solution (T0.2) in contrast with wild-type (WT). However, after setting membrane potential to -70 mV, T0.2 application similarly depolarized and increased action potential firing in Casr-/- and WT neurons. Enhanced activation of VGSCs was the dominant contributor to the depolarization and increase in excitability by T0.2 and occurred due to hyperpolarizing shifts in VGSC window currents. CaSR deletion depolarized VGSC window currents but did not affect NALCN activation. Regulation of VGSC gating by external divalents is the key mechanism mediating divalent-dependent changes in neocortical neuron 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.