Evidence map›Paper›PMID 27053114›Full record

ArticleScientific reports2016

The role of inositol 1,4,5-trisphosphate 3-kinase A in regulating emotional behavior and amygdala function.

Sooyoung Chung, Il Hwan Kim, Dongmin Lee, Kyungjoon Park, Joo Yeon Kim, Yeon Kyung Lee, Eun Joo Kim, Hyun Woo Lee, June-seek Choi, Gi Hoon Son and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  9. Functional New World monkey oxytocin forms elicit an altered signaling profile and promotes parental care in rats.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

13 authors at 4 institutions in 2 countries.

Sooyoung ChungDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
Il Hwan KimDepartment of Cell Biology, Duke University Medical School, Durham, North Carolina 27710, USA.
Dongmin LeeDepartment of Anatomy, College of Medicine, Korea University, Seoul 136-705, Korea.
Kyungjoon ParkDepartment of Biology, Department of Life and Nanopharmaceutical Sciences, Kyunghee University, Seoul 130-701, Korea.
Joo Yeon KimDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
Yeon Kyung LeeDepartment of Psychology, Korea University, Seoul 136-701, Korea.
Eun Joo KimDepartment of Psychology, University of Washington, Seattle, WA, USA.
Hyun Woo LeeDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
June-seek ChoiDepartment of Psychology, Korea University, Seoul 136-701, Korea.
Gi Hoon SonDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
Woong SunDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
Ki Soon ShinDepartment of Psychology, Korea University, Seoul 136-701, Korea.
Hyun KimDepartment of Biomedical Sciences, Brain Korea 21 PLUS, College of Medicine, Korea University, Seoul 136-705, Korea.
Korea University · KRDuke University · USKyung Hee University · KRUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) is a molecule enriched in the brain and neurons that regulates intracellular calcium levels via signaling through the inositol trisphosphate receptor. In the present study, we found that IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. Genetic abrogation of IP3K-A altered amygdala gene expression, particularly in genes involved in key intracellular signaling pathways and genes mediating fear- and anxiety-related behaviors. In agreement with the changes in amygdala gene expression profiles, IP3K-A knockout (KO) mice displayed more robust responses to aversive stimuli and spent less time in the open arms of the elevated plus maze, indicating high levels of innate fear and anxiety. In addition to behavioral phenotypes, decreased excitatory and inhibitory postsynaptic current and reduced c-Fos immunoreactivity in the CeA of IP3K-A KO mice suggest that IP3K-A has a profound influence on the basal activities of fear- and anxiety-mediating amygdala circuitry. In conclusion, our findings collectively demonstrate that IP3K-A plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala.

Indexed as

EmotionsAnimalsBehavior, AnimalCentral Amygdaloid NucleusGene Expression ProfilingGene Expression RegulationMaleMiceMice, KnockoutPhosphotransferases (Alcohol Group Acceptor)Signal TransductionInositol 1,4,5-trisphosphate 3-kinasePhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID27053114
PMCPMC4823716
OpenAlexW2316259849

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.