Linked Life Data

12865897

Source:http://linkedlifedata.com/resource/pubmed/id/12865897

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2003-9-25
pubmed:abstractText
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
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0893-133X
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1778-89
pubmed:dateRevised
2011-5-18
pubmed:meshHeading
pubmed-meshheading:12865897-Aging, pubmed-meshheading:12865897-Amphetamine, pubmed-meshheading:12865897-Animals, pubmed-meshheading:12865897-Central Nervous System Stimulants, pubmed-meshheading:12865897-Clozapine, pubmed-meshheading:12865897-Corpus Striatum, pubmed-meshheading:12865897-Disease Models, Animal, pubmed-meshheading:12865897-Dopamine, pubmed-meshheading:12865897-Dopamine Antagonists, pubmed-meshheading:12865897-Drug Interactions, pubmed-meshheading:12865897-Female, pubmed-meshheading:12865897-GABA Antagonists, pubmed-meshheading:12865897-Haloperidol, pubmed-meshheading:12865897-Hippocampus, pubmed-meshheading:12865897-Inhibition (Psychology), pubmed-meshheading:12865897-Interferon Inducers, pubmed-meshheading:12865897-Male, pubmed-meshheading:12865897-Motor Activity, pubmed-meshheading:12865897-Poly I-C, pubmed-meshheading:12865897-Pregnancy, pubmed-meshheading:12865897-Prenatal Exposure Delayed Effects, pubmed-meshheading:12865897-Rats, pubmed-meshheading:12865897-Rats, Wistar, pubmed-meshheading:12865897-Schizophrenia
pubmed:year
2003
pubmed:articleTitle
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.
pubmed:affiliation
Department of Psychology, Tel Aviv University, Tel Aviv, Israel.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't