Language:

Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6

The Journal of neuroscience, 2007-10, Vol.27 (40), p.10695-10702 [Peer Reviewed Journal]

Copyright © 2007 Society for Neuroscience 0270-6474/07/2710695-08$15.00/0 2007 ;ISSN: 0270-6474 ;EISSN: 1529-2401 ;DOI: 10.1523/JNEUROSCI.2178-07.2007 ;PMID: 17913903

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6
Author: Smith, Stephen E. P ; Li, Jennifer ; Garbett, Krassimira ; Mirnics, Karoly ; Patterson, Paul H
Subjects: Analysis of Variance ; Animals ; Antibodies - administration & dosage ; Behavior, Animal ; Brain - embryology ; Brain - immunology ; Cytokines - immunology ; Cytokines - metabolism ; Embryo, Mammalian ; Enzyme-Linked Immunosorbent Assay - methods ; Exploratory Behavior ; Female ; Fetal Development - physiology ; Interleukin-6 - deficiency ; Interleukin-6 - physiology ; Interpersonal Relations ; Lipopolysaccharides ; Maternal-Fetal Relations ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neural Inhibition - drug effects ; Neural Inhibition - physiology ; Oligonucleotide Array Sequence Analysis - methods ; Poly I-C ; Pregnancy ; Prenatal Exposure Delayed Effects - chemically induced ; Prenatal Exposure Delayed Effects - immunology
Is Part Of: The Journal of neuroscience, 2007-10, Vol.27 (40), p.10695-10702
Description: Schizophrenia and autism are thought to result from the interaction between a susceptibility genotype and environmental risk factors. The offspring of women who experience infection while pregnant have an increased risk for these disorders. Maternal immune activation (MIA) in pregnant rodents produces offspring with abnormalities in behavior, histology, and gene expression that are reminiscent of schizophrenia and autism, making MIA a useful model of the disorders. However, the mechanism by which MIA causes long-term behavioral deficits in the offspring is unknown. Here we show that the cytokine interleukin-6 (IL-6) is critical for mediating the behavioral and transcriptional changes in the offspring. A single maternal injection of IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) deficits in the adult offspring. Moreover, coadministration of an anti-IL-6 antibody in the poly(I:C) model of MIA prevents the PPI, LI, and exploratory and social deficits caused by poly(I:C) and normalizes the associated changes in gene expression in the brains of adult offspring. Finally, MIA in IL-6 knock-out mice does not result in several of the behavioral changes seen in the offspring of wild-type mice after MIA. The identification of IL-6 as a key intermediary should aid in the molecular dissection of the pathways whereby MIA alters fetal brain development, which can shed new light on the pathophysiological mechanisms that predispose to schizophrenia and autism.
Publisher: United States: Soc Neuroscience
Language: English
Identifier: ISSN: 0270-6474
EISSN: 1529-2401
DOI: 10.1523/JNEUROSCI.2178-07.2007
PMID: 17913903
Source: GFMER Free Medical Journals
MEDLINE
PubMed Central
Alma/SFX Local Collection

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6

Copyright © 2007 Society for Neuroscience 0270-6474/07/2710695-08$15.00/0 2007 ;ISSN: 0270-6474 ;EISSN: 1529-2401 ;DOI: 10.1523/JNEUROSCI.2178-07.2007 ;PMID: 17913903

Searching Remote Databases, Please Wait