Evidence map›Paper›PMID 22842147›Full record

ArticleNature neuroscience2012

Paradoxical contribution of SK3 and GIRK channels to the activation of mouse vomeronasal organ.

SangSeong Kim, Limei Ma, Kristi L Jensen, Michelle M Kim, Chris T Bond, John P Adelman, C Ron Yu

Abstract read
In one paragraph

Article in Nature neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Dopamine modulation of aggression.Psychopharmacology · 2026
    Review
  2. CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Article
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  8. Review
  9. Article
  10. CaThe Journal of biological chemistry · 2018
    Article
  11. Article
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  14. Article
  15. Article
  16. Review
  17. Genetic dissection of neural circuits underlying sexually dimorphic social behaviours.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  18. Article
  19. Review
  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

7 authors at 4 institutions in 1 country.

SangSeong KimStowers Institute for Medical Research, Kansas City, Missouri, USA.
Limei Ma
Kristi L Jensen
Michelle M Kim
Chris T Bond
John P Adelman
C Ron Yu
Stowers Institute for Medical Research · USVollum Institute · USColumbia University · USUniversity Medical Center · US

Funding

Molecular Physiology of the SK2 Channels in CA1 NeuronsR01NS038880 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAYLIE, JAMES G · 2000 to 2017
$6.0M
Genetic Mapping of Functional Vomeronasal CircuitsR01DC008003 · NIDCD · STOWERS INSTITUTE FOR MEDICAL RESEARCH · PI YU, CONGRONG RON · 2006 to 2020
$5.7M
Coupled LTP-dependent trafficking of synaptic SK channels and NMDARsR01MH093599 · NIMH · OREGON HEALTH & SCIENCE UNIVERSITY · PI ADELMAN, JOHN P, MAYLIE, JAMES G · 2012 to 2015
$1.2M
NIDCD NIH HHS R01 DC008003NIMH NIH HHS R01 MH093599NINDS NIH HHS R01 NS038880PHS HHS NIDCD 008003
6 · The paper itself

Abstract

The vomeronasal organ (VNO) is essential for intraspecies communication in many terrestrial vertebrates. The ionic mechanisms of VNO activation remain unclear. We found that the calcium-activated potassium channel SK3 and the G protein-activated potassium channel GIRK are part of an independent pathway for VNO activation. In slice preparations, the potassium channels attenuated inward currents carried by TRPC2 and calcium-activated chloride channels (CACCs). In intact tissue preparations, paradoxically, the potassium channels enhanced urine-evoked inward currents. This discrepancy resulted from the loss of a high concentration of lumenal potassium, which enabled the influx of potassium ions to depolarize the VNO neurons in vivo. Both Sk3 (also known as Kcnn3) and Girk1 (also known as Kcnj3) homozygous null mice showed deficits in mating and aggressive behaviors, and the deficiencies in Sk3(-/-) mice were exacerbated by Trpc2 knockout. Our results suggest that VNO activation is mediated by TRPC2, CACCs and two potassium channels, all of which contributed to the in vivo depolarization of VNO neurons.

Indexed as

AggressionAnimalsBehavior, AnimalDendritesFemaleFluorescent Antibody TechniqueG Protein-Coupled Inwardly-Rectifying Potassium ChannelsIn Situ HybridizationMaleMiceMice, Inbred C57BLMice, KnockoutMucusPatch-Clamp TechniquesPotassiumSexual Behavior, AnimalG Protein-Coupled Inwardly-Rectifying Potassium ChannelsKcnn3 protein, mousePotassiumSmall-Conductance Calcium-Activated Potassium ChannelsTrpc2 protein, mouseTRPC Cation Channels

Identifiers

PMID22842147
PMCPMC3431453
OpenAlexW2153041644

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.