Evidence map›Paper›PMID 24206670›Full record

ArticleNeuron2013

Disruption of dopamine neuron activity pattern regulation through selective expression of a human KCNN3 mutation.

Marta E Soden, Graham L Jones, Christina A Sanford, Amanda S Chung, Ali D Güler, Charles Chavkin, Rafael Luján, Larry S Zweifel

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Frontiers in neuroscience · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Autism-associated mutations in KProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018
    Review
  19. SK2 Channels Associate With mGluFrontiers in cellular neuroscience · 2018
    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

8 authors at 2 institutions in 2 countries.

Marta E SodenDepartment of Pharmacology, University of Washington, Seattle, WA 98195, USA; Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98195, USA.
Graham L Jones
Christina A Sanford
Amanda S Chung
Ali D Güler
Charles Chavkin
Rafael Luján
Larry S Zweifel
University of Washington · USUniversity of Castilla-La Mancha · ES

Funding

Pharmacological Sciences SupplementT32GM007750 · NIGMS · UNIVERSITY OF WASHINGTON · PI ATKINS, WILLIAM M · 1985 to 2023
$12.6M
Functional Mapping of Dopamine-Dependent Fear Circuitry Through Advanced GeneticR01MH094536 · NIMH · UNIVERSITY OF WASHINGTON · PI ZWEIFEL, LARRY S · 2011 to 2015
$2.3M
The molecular basis of emotional learningP30MH089887 · NIMH · UNIVERSITY OF WASHINGTON · PI NEUMAIER, JOHN F · 2009 to 2010
$1.4M
Dynorphins and Kappa Opioid Receptors in the Stress ResponseK05DA020570 · NIDA · UNIVERSITY OF WASHINGTON · PI CHAVKIN, CHARLES · 2006 to 2015
$1.2M
Howard Hughes Medical InstituteNIDA NIH HHS 5T32DA727817NIDA NIH HHS K05 DA020570NIDA NIH HHS KO5DA020570NIGMS NIH HHS T32 GM007750NIMH NIH HHS 1R01MH094536NIMH NIH HHS P30 MH089887NIMH NIH HHS P30MH089887NIMH NIH HHS R01 MH094536
6 · The paper itself

Abstract

The calcium-activated small conductance potassium channel SK3 plays an essential role in the regulation of dopamine neuron activity patterns. Here we demonstrate that expression of a human disease-related SK3 mutation (hSK3Δ) in dopamine neurons of mice disrupts the balance between tonic and phasic dopamine neuron activity. Expression of hSK3Δ suppressed endogenous SK currents, reducing coupling between SK channels and NMDA receptors (NMDARs) and increasing permissiveness for burst firing. Consistent with enhanced excitability of dopamine neurons, hSK3Δ increased evoked calcium signals in dopamine neurons in vivo and potentiated evoked dopamine release. Specific expression of hSK3Δ led to deficits in attention and sensory gating and heightened sensitivity to a psychomimetic drug. Sensory-motor alterations and psychomimetic sensitivity were recapitulated in a mouse model of transient, reversible dopamine neuron activation. These results demonstrate the cell-autonomous effects of a human ion channel mutation on dopamine neuron physiology and the impact of activity pattern disruption on behavior.

Indexed as

Action PotentialsAnimalsAttentionCalcium SignalingConditioning, ClassicalDependovirusDopamineDopaminergic NeuronsElectrophysiological PhenomenaExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsHallucinogensHumansImmunohistochemistryIn Vitro TechniquesMiceDopamineExcitatory Amino Acid AgonistsHallucinogensKCNN3 protein, humanN-MethylaspartateReceptors, N-Methyl-D-AspartateSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID24206670
PMCPMC3840077
OpenAlexW1971104810

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.