Home LiteratureArticle Details
PMID: 12865897 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't

Immune activation during pregnancy in rats leads to a postpubertal emergence of disrupted latent inhibition, dopaminergic hyperfunction, and altered limbic morphology in the offspring: a novel neurodevelopmental model of schizophrenia.

Zuckerman L, Rehavi M, Nachman R, Weiner I

Abstract

Prenatal exposure to infection is associated with increased liability to schizophrenia, and it is believed that such an association is mediated by the maternal immune response, in particular, the proinflammatory cytokines released by the maternal immune system, which may disrupt fetal brain development. Impaired capacity to ignore irrelevant stimuli is one of the central deficits in schizophrenia, and is manifested, among others, in loss of latent inhibition (LI), a phenomenon whereby repeated inconsequential pre-exposure to a stimulus impairs its subsequent capacity to signal significant consequences. We tested the effects of prenatal immune activation induced by peripheral administration of the synthetic cytokine releaser polyriboinosinic-polyribocytidilic acid (poly I : C) to pregnant dams, on LI in juvenile and adult offspring. Consistent with the characteristic maturational delay of schizophrenia, prenatal immune activation did not affect LI in the juvenile offspring, but led to LI disruption in adulthood. Both haloperidol (0.1 mg/kg) and clozapine (5 mg/kg) reinstated LI in the adult offspring. In addition, prenatal immune activation led to a postpubertal emergence of increased sensitivity to the locomotor-stimulating effects of amphetamine and increased in vitro striatal dopamine release, as well as to morphological alterations in the hippocampus and the entorhinal cortex in the adult offspring, consistent with the well-documented mesolimbic dopaminergic and temporolimbic pathology in schizophrenia. These results suggest that prenatal poly I : C administration may provide a neurodevelopmental model of schizophrenia that reproduces a putative inducing factor; mimics the temporal course as well as some central abnormalities of the disorder; and predicts responsiveness to antipsychotic drugs. Neuropsychopharmacology (2003) 28, 1778-1789. advance online publication, 16 July 2003; doi:10.1038/sj.npp.1300248

MeSH Terms
Aging Amphetamine/adverse effects Animals Central Nervous System Stimulants/adverse effects Clozapine/adverse effects Corpus Striatum/drug effects,metabolism Disease Models, Animal Dopamine/metabolism Dopamine Antagonists/adverse effects Drug Interactions Female GABA Antagonists/adverse effects Haloperidol/adverse effects Hippocampus/abnormalities,drug effects,pathology In Vitro Techniques Inhibition, Psychological Interferon Inducers/adverse effects Male Motor Activity/drug effects Poly I-C/adverse effects Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Schizophrenia/physiopathology
Chemicals
Central Nervous System Stimulants Dopamine Antagonists GABA Antagonists Interferon Inducers Amphetamine Clozapine Haloperidol Poly I-C Dopamine
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Zuckerman Lee
Department of Psychology, Tel Aviv University, Tel Aviv, Israel.
Rehavi Moshe
Nachman Rachel
Weiner Ina
Article Info
Journal
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
Abbr.
Neuropsychopharmacology
ISSN
0893-133X
Published
2003-10-00
Pages
1778-89
Language
English
Region
England
NLM ID
8904907
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]