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Does prenatal exposure to influenza in mice induce pyramidal cell disarray in the dorsal hippocampus?

Identifieur interne : 001D17 ( Main/Exploration ); précédent : 001D16; suivant : 001D18

Does prenatal exposure to influenza in mice induce pyramidal cell disarray in the dorsal hippocampus?

Auteurs : David Cotter [Irlande (pays)] ; Noriyoshi Takei [Royaume-Uni] ; Michael Farrell [Irlande (pays)] ; Pak Sham [Royaume-Uni] ; Peter Quinn [Royaume-Uni] ; Conall Larkin [Irlande (pays)] ; John Oxford [Irlande (pays)] ; Robin M. Murray [Royaume-Uni] ; Eadbhard O'Callaghan [Irlande (pays)]

Source :

RBID : ISTEX:54D50F290DF4C42758D42422E86E3945B4E4C14F

Descripteurs français

English descriptors

Abstract

Abstract: Epidemiological studies point to an association between prenatal exposure to influenza and later schizophrenia. Such studies are consistent with neuropathologic reports demonstrating cytoarchitectural abnormalities in the hippocampus and parahippocampal gyrus suggestive of second trimester developmental anomalies. The hypothesis that prenatal exposure to influenza in the second trimester may induce hippocampal pyramidal cell disarray in mice was investigated. Between days 9–16 of pregnancy, 35 Balb/c mice were intranasally inoculated with either a mouse-adapted or non mouse-adapted pool of Influenza A/Singapore/1/57 (H2N2), and 10 controls were inoculated with normal saline. Offspring were sacrificed on day 21 postpartum. Microscopic examination of the CA1-CA2 junctional areas in the offspring of mice exposed to influenza failed to demonstrate excess pyramidal cell disarray when compared with influenza-free, age matched controls. There was evidence that disarray was greater among those exposed on day 13 of pregnancy. Analyses of the data by sex and severity of maternal infection failed to reveal any significant effects.

Url:
DOI: 10.1016/0920-9964(94)E0082-I


Affiliations:


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<term>Developmental disorder</term>
<term>Disease Models, Animal</term>
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<term>Etiology</term>
<term>Female</term>
<term>Hippocampus (pathology)</term>
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<term>Mice</term>
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<term>Orthomyxoviridae Infections (pathology)</term>
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<term>Prenatal Exposure Delayed Effects</term>
<term>Psychosis</term>
<term>Pyramidal Cells (pathology)</term>
<term>Pyramidal neuron</term>
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<term>Schizophrenia</term>
<term>Second trimester</term>
<term>Vulnerability</term>
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<term>Animaux</term>
<term>Cellules pyramidales (anatomopathologie)</term>
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<term>Femelle</term>
<term>Grossesse</term>
<term>Hippocampe (anatomopathologie)</term>
<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
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<term>Orthomyxoviridae Infections</term>
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<term>Disease Models, Animal</term>
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<term>Influenza A virus</term>
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<term>Encéphale pathologie</term>
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<term>Basal side</term>
<term>Bilateral phenomenon</term>
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<term>Cell orientation</term>
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<term>Complement fixation test</term>
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<term>Control groups</term>
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<term>Dorsal hippocampus</term>
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<term>Gestation</term>
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<term>Interface</term>
<term>Interface zone</term>
<term>Interface zones</term>
<term>Intranasal route</term>
<term>Junctional area</term>
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<term>Litter size</term>
<term>Long axis</term>
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<term>Maternal influenza</term>
<term>Maternal influenza infection</term>
<term>Monozygotic twins</term>
<term>Morphometric study</term>
<term>Neural tube defects</term>
<term>Neuron</term>
<term>Neuron formation</term>
<term>Neuronal migration</term>
<term>Normal saline</term>
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<term>Overall effect</term>
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<term>Prenatal exposure</term>
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<term>Schizophrenia</term>
<term>Schizophrenic patients</term>
<term>Second trimester</term>
<term>Sham</term>
<term>Similar placental unit</term>
<term>Specific vulnerability</term>
<term>Subsequent development</term>
<term>Such studies</term>
<term>Takei</term>
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<term>Vaginal plug</term>
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<front>
<div type="abstract" xml:lang="en">Abstract: Epidemiological studies point to an association between prenatal exposure to influenza and later schizophrenia. Such studies are consistent with neuropathologic reports demonstrating cytoarchitectural abnormalities in the hippocampus and parahippocampal gyrus suggestive of second trimester developmental anomalies. The hypothesis that prenatal exposure to influenza in the second trimester may induce hippocampal pyramidal cell disarray in mice was investigated. Between days 9–16 of pregnancy, 35 Balb/c mice were intranasally inoculated with either a mouse-adapted or non mouse-adapted pool of Influenza A/Singapore/1/57 (H2N2), and 10 controls were inoculated with normal saline. Offspring were sacrificed on day 21 postpartum. Microscopic examination of the CA1-CA2 junctional areas in the offspring of mice exposed to influenza failed to demonstrate excess pyramidal cell disarray when compared with influenza-free, age matched controls. There was evidence that disarray was greater among those exposed on day 13 of pregnancy. Analyses of the data by sex and severity of maternal infection failed to reveal any significant effects.</div>
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