ArticleNeuron2010
Extracellular calcium controls background current and neuronal excitability via an UNC79-UNC80-NALCN cation channel complex.
Article in Neuron, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 213 citations in OpenAlex.
- Divalent cation depletion enhances intrinsic neuronal excitability through CaSR-dependent modulation of threshold ion channels.PNAS nexus · 2026Article
- The NALCN channel complex is necessary for stabilizing sleep in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2026Article
- Supraphysiological Doses of Vitamin A Promote Changes in Hippocampal Oscillation Bands and Cardiac Activity in Wistar Rats.ACS omega · 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
- NaThe Journal of membrane biology · 2026Article
- Activation of CaExperimental brain research · 2025Article
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- Cadherin-16 regulates acoustic sensory gating in zebrafish through endocrine signaling.PLoS biology · 2025Article
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- The Biphasic Effect of Lipopolysaccharide on Membrane Potential.Membranes · 2025Article
- Intermittent fasting reprograms the brain proteome to prevent synaptic degeneration and cognitive impairment in vascular dementia.Theranostics · 2025Article
- Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat.Journal of neurochemistry · 2025Article
- The background sodium leak channel NALCN is a major controlling factor in pituitary cell excitability.The Journal of physiology · 2025Article
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- Systematized Serendipity: Fishing Expeditions for Anesthetic Drugs and Targets.Anesthesiology · 2024Review
- Cadherin 16 promotes sensory gating via the endocrine corpuscles of Stannius.bioRxiv : the preprint server for biology · 2024Article
- Imbalance inInternational journal of molecular sciences · 2024Article
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- Thallium's Threat to Aquatic Life: Stage-Specific Toxicity in Zebrafish Embryos and Larvae.Environment & health (Washington, D.C.) · 2024Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
In contrast to its extensively studied intracellular roles, the molecular mechanisms by which extracellular Ca(2+) regulates the basal excitability of neurons are unclear. One mechanism is believed to be through Ca(2+)'s interaction with the negative charges on the cell membrane (the charge screening effect). Here we show that, in cultured hippocampal neurons, lowering [Ca(2+)](e) activates a NALCN channel-dependent Na(+)-leak current (I(L-Na)). The coupling between [Ca(2+)](e) and NALCN requires a Ca(2+)-sensing G protein-coupled receptor, an activation of G-proteins, an UNC80 protein that bridges NALCN to a large novel protein UNC79 in the same complex, and the last amino acid of NALCN's intracellular tail. In neurons from nalcn and unc79 knockout mice, I(L-Na) is insensitive to changes in [Ca(2+)](e), and reducing [Ca(2+)](e) fails to elicit the excitatory effects seen in the wild-type. Therefore, extracellular Ca(2+) influences neuronal excitability through the UNC79-UNC80-NALCN complex in a G protein-dependent fashion.
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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.