Evidence map›Paper›PMID 24618690›Full record

ArticleTranslational psychiatry2014

Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse offspring.

T Uchida, T Furukawa, S Iwata, Y Yanagawa, A Fukuda

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.4field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  17. Frontiers in aging neuroscience · 2021
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  18. Behavioral Consequences of a Combination ofFrontiers in pharmacology · 2021
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  19. Anti-Stress Properties of Atypical Antipsychotics.Pharmaceuticals (Basel, Switzerland) · 2020
    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

5 authors at 2 institutions in 1 country.

T UchidaDepartment of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
T FurukawaDepartment of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
S IwataDepartment of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Y YanagawaDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
A FukudaDepartment of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hamamatsu University School of Medicine · JPGunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to maternal stress (MS) and mutations in GAD1, which encodes the γ-aminobutyric acid (GABA) synthesizing enzyme glutamate decarboxylase (GAD) 67, are both risk factors for psychiatric disorders. However, the relationship between these risk factors remains unclear. Interestingly, the critical period of MS for psychiatric disorders in offspring corresponds to the period of GABAergic neuron neurogenesis and migration in the fetal brain, that is, in the late stage of gestation. Indeed, decrement of parvalbumin (PV)-positive GABAergic interneurons in the medial prefrontal cortex (mPFC) and hippocampus (HIP) has often been observed in schizophrenia patients. In the present study, we used GAD67-green fluorescent protein (GFP) knock-in mice (that is, mice in which the Gad1 gene is heterozygously deleted; GAD67(+/GFP)) that underwent prenatal stress from embryonic day 15.0 to 17.5 and monitored PV-positive GABAergic neurons to address the interaction between Gad1 disruption and stress. Administration of 5-bromo-2-deoxyuridine revealed that neurogenesis of GFP-positive GABAergic neurons, but not cortical plate cells, was significantly diminished in fetal brains during MS. Differential expression of glucocorticoid receptors by different progenitor cell types may underlie this differential outcome. Postnatally, the density of PV-positive, but not PV-negative, GABAergic neurons was significantly decreased in the mPFC, HIP and somatosensory cortex but not in the motor cortex of GAD67(+/GFP) mice. By contrast, these findings were not observed in wild-type (GAD67(+/+)) offspring. These results suggest that prenatal stress, in addition to heterozygous deletion of Gad1, could specifically disturb the proliferation of neurons destined to be PV-positive GABAergic interneurons.

Indexed as

Gene-Environment InteractionAnimalsCerebral CortexFemaleGABAergic NeuronsGlutamate DecarboxylaseInterneuronsMiceMice, TransgenicNeurogenesisParvalbuminsPregnancyPrenatal Exposure Delayed EffectsReceptors, GlucocorticoidRisk FactorsStress, PsychologicalGlutamate Decarboxylaseglutamate decarboxylase 1ParvalbuminsReceptors, Glucocorticoid

Identifiers

PMID24618690
PMCPMC3966041
OpenAlexW2043644762

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.