Evidence map›Paper›PMID 27452469›Full record

ArticleCell reports2016

β-Arrestin-Dependent Dopaminergic Regulation of Calcium Channel Activity in the Axon Initial Segment.

Sungchil Yang, Roy Ben-Shalom, Misol Ahn, Alayna T Liptak, Richard M van Rijn, Jennifer L Whistler, Kevin J Bender

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. β-arrestins Are Scaffolding Proteins Required for Shh-Mediated Axon Guidance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  9. Arrestin-3 Agonism at Dopamine DBiological psychiatry · 2023
    Article
  10. Axon Initial Segment GABA Inhibits Action Potential Generation throughout Periadolescent Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Functional Microstructure of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. The β-arrestin-biased β-adrenergic receptor blocker carvedilol enhances skeletal muscle contractility.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Review
  20. Subcellular control of membrane excitability in the axon.Current opinion in neurobiology · 2019
    Review
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

7 authors at 3 institutions in 1 country.

Sungchil YangCenter for Integrative Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Alcohol and Addiction Research Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Roy Ben-ShalomCenter for Integrative Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Alcohol and Addiction Research Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Misol AhnDepartment of Pathology and Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA 94158, USA.
Alayna T LiptakCenter for Integrative Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Alcohol and Addiction Research Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Richard M van RijnDepartment of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907, USA.
Jennifer L WhistlerAlcohol and Addiction Research Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Kevin J BenderCenter for Integrative Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Alcohol and Addiction Research Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: kevin.bender@ucsf.edu.
Alcohol Research Group · USPurdue University West Lafayette · USUniversity of California, San Francisco · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MESSING, ROBERT O. · 2008 to 2017
$13.9M
Molecular and circuit mechanisms of antipsychoticsR01MH112729 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J, WHISTLER, JENNIFER L · 2017 to 2021
$2.6M
Dopamine receptor trafficking in drug sensitization and behavioral flexibilityR01DA037963 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WHISTLER, JENNIFER L · 2015 to 2019
$1.8M
Cellular mechanisms for dopaminergic control of learning in prefrontal cortexR01DA035913 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J · 2013 to 2017
$1.7M
Function and regulation of action potential bursts in the auditory system.R00DC011080 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J · 2012 to 2014
$734k
Development of a preclinical candidate for the treatment of alcoholismR00AA020539 · NIAAA · PURDUE UNIVERSITY · PI VAN RIJN, RICHARD M. · 2013 to 2015
$728k
Towards a unified model of action potential generationF32NS095580 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BEN-SHALOM, ROY · 2015 to 2018
$172k
NIAAA NIH HHS P50 AA017072NIAAA NIH HHS R00 AA020539NIDA NIH HHS R01 DA035913NIDA NIH HHS R01 DA037963NIDCD NIH HHS R00 DC011080NIMH NIH HHS R01 MH112729NINDS NIH HHS F32 NS095580
6 · The paper itself

Abstract

G-protein-coupled receptors (GPCRs) initiate a variety of signaling cascades, depending on effector coupling. β-arrestins, which were initially characterized by their ability to "arrest" GPCR signaling by uncoupling receptor and G protein, have recently emerged as important signaling effectors for GPCRs. β-arrestins engage signaling pathways that are distinct from those mediated by G protein. As such, arrestin-dependent signaling can play a unique role in regulating cell function, but whether neuromodulatory GPCRs utilize β-arrestin-dependent signaling to regulate neuronal excitability remains unclear. Here, we find that D3 dopamine receptors (D3R) regulate axon initial segment (AIS) excitability through β-arrestin-dependent signaling, modifying CaV3 voltage dependence to suppress high-frequency action potential generation. This non-canonical D3R signaling thereby gates AIS excitability via pathways distinct from classical GPCR signaling pathways.

Indexed as

AnimalsAxon Initial Segmentbeta-ArrestinsCalciumCalcium ChannelsDopamineHEK293 CellsHumansPhosphorylationReceptors, G-Protein-Coupledbeta-ArrestinsCalciumCalcium ChannelsDopamineReceptors, G-Protein-Coupled

Identifiers

PMID27452469
PMCPMC5074334
OpenAlexW2496255268

What OpenQuestion holds

Textmetadata
LicenceTDM
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.