Evidence map›Paper›PMID 25683697›Full record

ArticleBrain, behavior, and immunity2015

The interaction between maternal immune activation and alpha 7 nicotinic acetylcholine receptor in regulating behaviors in the offspring.

Wei-Li Wu, Catherine E Adams, Karen E Stevens, Ke-Huan Chow, Robert Freedman, Paul H Patterson

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

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  19. Astroglia in Autism Spectrum Disorder.International journal of molecular sciences · 2021
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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 3 institutions in 1 country.

Wei-Li WuDivision of Biology and Biological Engineering, California Institute of Technology, 1200 E. California Blvd., Pasadena, CA 91125, USA. Electronic address: wlwu@caltech.edu.
Catherine E AdamsDenver VA Medical Center, 1055 Clermont St., Denver, CO 80220, USA; Department of Psychiatry, University of Colorado Denver Anschutz Medical Campus, 12800 E. 19th Ave., Aurora, CO 80045, USA.
Karen E StevensDepartment of Psychiatry, University of Colorado Denver Anschutz Medical Campus, 12800 E. 19th Ave., Aurora, CO 80045, USA.
Ke-Huan ChowDivision of Biology and Biological Engineering, California Institute of Technology, 1200 E. California Blvd., Pasadena, CA 91125, USA.
Robert FreedmanDepartment of Psychiatry, University of Colorado Denver Anschutz Medical Campus, 12800 E. 19th Ave., Aurora, CO 80045, USA.
Paul H PattersonDivision of Biology and Biological Engineering, California Institute of Technology, 1200 E. California Blvd., Pasadena, CA 91125, USA.
California Institute of Technology · USUniversity of Colorado Anschutz Medical Campus · USDenver VA Medical Center · US

Funding

STATISTICAL GENETICS AND TREATMENT ANALYSISP50MH086383 · NIMH · UNIVERSITY OF COLORADO DENVER · PI FREEDMAN, ROBERT · 2009 to 2013
$10.6M
Autism Speaks AS7670NIMH NIH HHS 5P50MH086383-04NIMH NIH HHS P50 MH086383
6 · The paper itself

Abstract

Mutation of human chromosome 15q13.3 increases the risk for autism and schizophrenia. One of the noteworthy genes in 15q13.3 is CHRNA7, which encodes the nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) associated with schizophrenia in clinical studies and rodent models. This study investigates the role of α7nAChR in maternal immune activation (MIA) mice model, a murine model of environmental risk factor for autism and schizophrenia. We provided choline, a selective α7nAChR agonist among its several developmental roles, in the diet of C57BL/6N wild-type dams throughout the gestation and lactation period and induced MIA at mid-gestation. The adult offspring behavior and gene expression profile in the maternal-placental-fetal axis at mid-gestation were investigated. We found that choline supplementation prevented several MIA-induced behavioral abnormalities in the wild-type offspring. Pro-inflammatory cytokine interleukin-6 (Il6) and Chrna7 gene expression in the wild-type fetal brain were elevated by poly(I:C) injection and were suppressed by gestational choline supplementation. We further investigated the gene expression level of Il6 in Chrna7 mutant mice. We found that the basal level of Il6 was higher in Chrna7 mutant fetal brain, which suggests that α7nAChR may serve an anti-inflammatory role in the fetal brain during development. Lastly, we induced MIA in Chrna7(+/-) offspring. The Chrna7(+/-) offspring were more vulnerable to MIA, with increased behavioral abnormalities. Our study shows that α7nAChR modulates inflammatory response affecting the fetal brain and demonstrates its effects on offspring behavior development after MIA.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsAutistic DisorderBehavior, AnimalCholineDisease Models, AnimalFemaleMiceMice, Inbred C57BLPregnancyPrenatal Exposure Delayed EffectsSchizophreniaalpha7 Nicotinic Acetylcholine ReceptorCholineAutismCholine supplementationInterleukin-6 (IL-6)Maternal immune activation (MIA)Maternal infectionNicotinic acetylcholine receptor alpha 7 subunit (α7AChR, CHRNA7, Chrna7)Poly(I:C)Schizophrenia

Identifiers

PMID25683697
PMCPMC4414803
OpenAlexW1999172174

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.