ArticleeLife2018
G
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
41 citing papers in PubMed, 82 citations in OpenAlex.
- Deletion of the sodium leak channel NALCN in dopamine neurons alters D2R-mediated signalling and psychostimulant responsiveness.The Journal of physiology · 2026Article
- The sodium leak channel NALCN in Drd2Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Rebound Bursting Selectively Enables Fast Dynamics in Dopamine Midbrain Neurons Projecting to the Dorsolateral Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A switch in kappa opioid receptor signaling from inhibitory to excitatory induced by stress in a subset of cortically-projecting dopamine neurons.bioRxiv : the preprint server for biology · 2025Article
- Molecular Determinants of A9 Dopaminergic Neurons.Neuromolecular medicine · 2025Review
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- The background sodium leak channel NALCN is a major controlling factor in pituitary cell excitability.The Journal of physiology · 2025Article
- Article
- The NaeLife · 2024Article
- NALCN Channels Are Not Major targets of GαmicroPublication biology · 2024Article
- The NabioRxiv : the preprint server for biology · 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
- The Concise Guide to PHARMACOLOGY 2023/24: Ion channels.British journal of pharmacology · 2023Article
- Angiotensin ATCell reports · 2023Article
- RGS6 negatively regulates inhibitory G protein signaling in dopamine neurons and positively regulates binge-like alcohol consumption in mice.British journal of pharmacology · 2023Article
- Potentiation of neuronal activity by tonic GluD1 current in brain slices.EMBO reports · 2023Article
- Article
- Dendritic involvement in inhibition and disinhibition of vulnerable dopaminergic neurons in healthy and pathological conditions.Neurobiology of disease · 2022Review
- Researching Mitigation of Alcohol Binge Drinking in Polydrug Abuse: KCNK13 and RASGRF2 Gene(s) Risk Polymorphisms Coupled with Genetic Addiction Risk Severity (GARS) Guiding Precision Pro-Dopamine Regulation.Journal of personalized medicine · 2022Article
- Differential modulation of C. elegans motor behavior by NALCN and two-pore domain potassium channels.PLoS genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dopamine (D2) receptors provide autoinhibitory feedback onto dopamine neurons through well-known interactions with voltage-gated calcium channels and G protein-coupled inwardly-rectifying potassium (GIRK) channels. Here, we reveal a third major effector involved in D2R modulation of dopaminergic neurons - the sodium leak channel, NALCN. We found that activation of D2 receptors robustly inhibits isolated sodium leak currents in wild-type mice but not in NALCN conditional knockout mice. Intracellular GDP-βS abolished the inhibition, indicating a G protein-dependent signaling mechanism. The application of dopamine reliably slowed pacemaking even when GIRK channels were pharmacologically blocked. Furthermore, while spontaneous activity was observed in nearly all dopaminergic neurons in wild-type mice, neurons from NALCN knockouts were mainly silent. Both observations demonstrate the critical importance of NALCN for pacemaking in dopaminergic neurons. Finally, we show that GABA-B receptor activation also produces inhibition of NALCN-mediated currents. Therefore, we identify NALCN as a core effector of inhibitory G protein-coupled receptors.
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What OpenQuestion holds
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.