Evidence map›Paper›PMID 21233214›Full record

ArticleThe Journal of biological chemistry2011

Contribution of Kv1.2 voltage-gated potassium channel to D2 autoreceptor regulation of axonal dopamine overflow.

Stephanie Fulton, Dominic Thibault, Jose A Mendez, Nicolas Lahaie, Emanuele Tirotta, Emiliana Borrelli, Michel Bouvier, Bruce L Tempel, Louis-Eric Trudeau

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
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  8. Article
  9. Article
  10. Caged ZnACS chemical neuroscience · 2024
    Article
  11. Review
  12. Article
  13. The potassium channel auxiliary subunit Kvβ2 (Journal of neurophysiology · 2022
    Article
  14. Article
  15. Article
  16. Potassium Channels and Their Potential Roles in Substance Use Disorders.International journal of molecular sciences · 2021
    Review
  17. Review
  18. Review
  19. Article
  20. Article
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

9 authors at 5 institutions in 3 countries.

Stephanie FultonDepartment of Pharmacology and Groupe de Recherche sur le Système Nerveux Central, Université de Montréal, Quebec H3C 3J7, Canada.
Dominic Thibault
Jose A Mendez
Nicolas Lahaie
Emanuele Tirotta
Emiliana Borrelli
Michel Bouvier
Bruce L Tempel
Louis-Eric Trudeau
Nerve Centre · GBUniversity of California, Irvine · USInstitute for Research in Immunology and Cancer · CAUniversité de Montréal · CAUniversity of Washington · US

Funding

GENETIC MODEL FOR CONGENITAL DEAFNESSR01DC002739 · NIDCD · UNIVERSITY OF WASHINGTON · PI TEMPEL, BRUCE L · 1995 to 2013
$4.1M
Presynaptic versus postsynaptic functions of dopamine D2 receptors in the responsR01DA024689 · NIDA · UNIVERSITY OF CALIFORNIA-IRVINE · PI BORRELLI, EMILIANA · 2008 to 2012
$1.7M
CIHR MOP-10501CIHR MOP-49591NIDA NIH HHS DA024689NIDA NIH HHS R01 DA024689NIDCD NIH HHS R01 DC002739NIDCD NIH HHS R01-DC002739
6 · The paper itself

Abstract

Impairments in axonal dopamine release are associated with neurological disorders such as schizophrenia and attention deficit hyperactivity disorder and pathophysiological conditions promoting drug abuse and obesity. The D2 dopamine autoreceptor (D2-AR) exerts tight regulatory control of axonal dopamine (DA) release through a mechanism suggested to involve K(+) channels. To evaluate the contribution of Kv1 voltage-gated potassium channels of the Shaker gene family to the regulation of axonal DA release by the D2-AR, the present study employed expression analyses, real time measurements of striatal DA overflow, K(+) current measurements and immunoprecipitation assays. Kv1.1, -1.2, -1.3, and -1.6 mRNA and protein were detected in midbrain DA neurons purified by fluorescence-activated cell sorting and in primary DA neuron cultures. In addition, Kv1.1, -1.2, and -1.6 were localized to DA axonal processes in the dorsal striatum. By means of fast scan cyclic voltammetry in striatal slice preparations, we found that the inhibition of stimulation-evoked DA overflow by a D2 agonist was attenuated by Kv1.1, -1.2, and -1.6 toxin blockers. A particular role for the Kv1.2 subunit in the process whereby axonal D2-AR inhibits DA overflow was established with the use of a selective Kv1.2 blocker and Kv1.2 knock-out mice. Moreover, we demonstrate the ability of D2-AR activation to increase Kv1.2 currents in co-transfected cells and its reliance on Gβγ subunit signaling along with the physical coupling of D2-AR and Kv1.2-containing channels in striatal tissue. These findings underline the contribution of Kv1.2 in the regulation of nigrostriatal DA release by the D2-AR and thereby offer a novel mechanism by which DA release is regulated.

Indexed as

AnimalsAxonsCorpus StriatumDopamineDopamine AgonistsKv1.2 Potassium ChannelMaleMiceMice, KnockoutReceptors, Dopamine D2Signal TransductionDopamineDopamine AgonistsKv1.2 Potassium ChannelReceptors, Dopamine D2

Identifiers

PMID21233214
PMCPMC3059064
OpenAlexW2033712681

What OpenQuestion holds

Textmetadata
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.