Evidence map›Paper›PMID 27177420›Full record

ArticleeLife2016

The leak channel NALCN controls tonic firing and glycolytic sensitivity of substantia nigra pars reticulata neurons.

Andrew Lutas, Carolina Lahmann, Magali Soumillon, Gary Yellen

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 97 citations in OpenAlex.

  1. The sodium leak channel NALCN in Drd2Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Synaptic integration and competition in the substantia nigra pars reticulata-An experimental and in silico analysis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Rho signaling promotes cell excitability and synaptic transmission.bioRxiv : the preprint server for biology · 2025
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  11. The NaeLife · 2024
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  12. NALCN Channels Are Not Major targets of GαmicroPublication biology · 2024
    Article
  13. The NabioRxiv : the preprint server for biology · 2023
    Article
  14. Article
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  16. Effects of NALCN-Encoded NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Andrew LutasDepartment of Neurobiology, Harvard Medical School, Boston, United States.ORCID 0000-0002-6991-2898
Carolina LahmannDepartment of Neurobiology, Harvard Medical School, Boston, United States.
Magali SoumillonBroad Institute, Cambridge, United States.
Gary YellenDepartment of Neurobiology, Harvard Medical School, Boston, United States.ORCID 0000-0003-4228-7866
Boston University · USBroad Institute · US

Funding

Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZHIGANG HE · 1998 to 2026
$21.3M
Super-Resolution ImagingP30NS072030 · NINDS · HARVARD MEDICAL SCHOOL · PI REGEHR, WADE G · 2011 to 2020
$5.8M
Single cell analysis of metabolism using genetically-encoded fluorescent sensorsDP1EB016985 · NIBIB · HARVARD MEDICAL SCHOOL · PI YELLEN, GARY I · 2012 to 2016
$4.2M
Cellular mechanisms of dietary therapy for epilepsyR01NS055031 · NINDS · HARVARD MEDICAL SCHOOL · PI YELLEN, GARY I · 2008 to 2016
$3.2M
Metabolic and KATP channel regulation of the cortical slow oscillationF31NS077633 · NINDS · HARVARD MEDICAL SCHOOL · PI LUTAS, ANDREW · 2011 to 2013
$94k
NIBIB NIH HHS DP1 EB016985NINDS NIH HHS F31 NS077633NINDS NIH HHS P30 NS072030NINDS NIH HHS R01 NS055031
6 · The paper itself

Abstract

Certain neuron types fire spontaneously at high rates, an ability that is crucial for their function in brain circuits. The spontaneously active GABAergic neurons of the substantia nigra pars reticulata (SNr), a major output of the basal ganglia, provide tonic inhibition of downstream brain areas. A depolarizing 'leak' current supports this firing pattern, but its molecular basis remains poorly understood. To understand how SNr neurons maintain tonic activity, we used single-cell RNA sequencing to determine the transcriptome of individual mouse SNr neurons. We discovered that SNr neurons express the sodium leak channel, NALCN, and that SNr neurons lacking NALCN have impaired spontaneous firing. In addition, NALCN is involved in the modulation of excitability by changes in glycolysis and by activation of muscarinic acetylcholine receptors. Our findings suggest that disruption of NALCN could impair the basal ganglia circuit, which may underlie the severe motor deficits in humans carrying mutations in NALCN.

Indexed as

Action PotentialsGlycolysisAnimalsGABAergic NeuronsGene Expression ProfilingIon ChannelsMembrane ProteinsMiceNerve Tissue ProteinsPars ReticulataSequence Analysis, RNASingle-Cell AnalysisIon ChannelsMembrane ProteinsNALCN protein, mouseNerve Tissue Proteinsbasal ganglialeak currentmetabolism and excitabilitymouseneurosciencespontaneous firing

Identifiers

PMID27177420
PMCPMC4902561
OpenAlexW2387268774

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.