Evidence map›Paper›PMID 31275123›Full record

ArticleFrontiers in behavioral neuroscience2019

Loss of Glutamate Decarboxylase 67 in Somatostatin-Expressing Neurons Leads to Anxiety-Like Behavior and Alteration in the Akt/GSK3β Signaling Pathway.

Shigeo Miyata, Ryota Kumagaya, Toshikazu Kakizaki, Kazuyuki Fujihara, Kaori Wakamatsu, Yuchio Yanagawa

Open access · goldAbstract read
In one paragraph

Article in Frontiers in behavioral neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Growth Hormone Action in Somatostatin Neurons Regulates Anxiety and Fear Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  5. Article
  6. The Molecular Gut-Brain Axis in Early Brain Development.International journal of molecular sciences · 2022
    Review
  7. Article
  8. GABAergic deficits in absence of LPABrain structure & function · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Behavioral Consequences of a Combination ofFrontiers in pharmacology · 2021
    Article
  13. Article
  14. Article
  15. 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

6 authors at 2 institutions in 1 country.

Shigeo MiyataDepartment of Genetic and Behavioral Neuroscience, Graduate School of Medicine, Gunma University, Maebashi, Japan.
Ryota KumagayaDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu, Japan.
Toshikazu KakizakiDepartment of Genetic and Behavioral Neuroscience, Graduate School of Medicine, Gunma University, Maebashi, Japan.
Kazuyuki FujiharaDepartment of Genetic and Behavioral Neuroscience, Graduate School of Medicine, Gunma University, Maebashi, Japan.
Kaori WakamatsuDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu, Japan.
Yuchio YanagawaDepartment of Genetic and Behavioral Neuroscience, Graduate School of Medicine, Gunma University, Maebashi, Japan.
Gunma University · JPKiryu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is a highly prevalent psychiatric disorder worldwide. Several lines of evidence suggest that the dysfunction of somatostatin (SOM) neurons is associated with the pathophysiology of MDD. Importantly, most SOM neurons are γ-aminobutyric acid (GABA) interneurons. However, whether the dysfunction of GABAergic neurotransmission from SOM neurons contributes to the pathophysiology of MDD remains elusive. To address this issue, we investigated the emotional behaviors and relevant molecular mechanism in mice lacking glutamate decarboxylase 67 (GAD67), an isoform of GABA-synthesizing enzyme, specifically in SOM neurons (SOM-GAD67 mice). The SOM-GAD67 mice exhibited anxiety-like behavior in the open-field test without an effect on locomotor activity. The SOM-GAD67 mice showed depression-like behavior in neither the forced swimming test nor the sucrose preference test. In addition, the ability to form contextual fear memory was normal in the SOM-GAD67 mice. Furthermore, the plasma corticosterone level was normal in the SOM-GAD67 mice both under baseline and stress conditions. The expression ratios of p-Akt

Indexed as

AktanxietydepressionGABAGADGSK3βsomatostatin

Identifiers

PMID31275123
PMCPMC6591520
OpenAlexW2949395283

What OpenQuestion holds

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LicenceCC BY
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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.