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Tytuł pozycji:

Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies.

Tytuł:
Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies.
Autorzy:
Giovanoli S; Physiology and Behavior Laboratory, ETH Zurich, Schwerzenbach, Switzerland.
Weber-Stadlbauer U; Physiology and Behavior Laboratory, ETH Zurich, Schwerzenbach, Switzerland; Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
Schedlowski M; Institute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Meyer U; Physiology and Behavior Laboratory, ETH Zurich, Schwerzenbach, Switzerland; Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland. Electronic address: .
Engler H; Institute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Źródło:
Brain, behavior, and immunity [Brain Behav Immun] 2016 Jul; Vol. 55, pp. 25-38. Date of Electronic Publication: 2015 Sep 25.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: <2000- > : Amsterdam : Elsevier
Original Publication: San Diego : Academic Press, [c1987-
MeSH Terms:
Hippocampus/*immunology
Hippocampus/*physiopathology
Interleukin-1beta/*metabolism
Prenatal Exposure Delayed Effects/*immunology
Prenatal Exposure Delayed Effects/*physiopathology
Age Factors ; Animals ; Disease Models, Animal ; Female ; Immunologic Factors/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/immunology ; Microglia/metabolism ; Poly I-C/pharmacology ; Pregnancy
Contributed Indexing:
Keywords: Autism; Cytokines; Inflammation; Maternal immune activation; Microglia; Poly(I:C); Schizophrenia; Synapse
Substance Nomenclature:
0 (IL1B protein, mouse)
0 (Immunologic Factors)
0 (Interleukin-1beta)
O84C90HH2L (Poly I-C)
Entry Date(s):
Date Created: 20150927 Date Completed: 20171229 Latest Revision: 20171230
Update Code:
20240104
DOI:
10.1016/j.bbi.2015.09.015
PMID:
26408796
Czasopismo naukowe
Prenatal exposure to infectious or inflammatory insults can increase the risk of developing neuropsychiatric disorder in later life, including schizophrenia, bipolar disorder, and autism. These brain disorders are also characterized by pre- and postsynaptic deficits. Using a well-established mouse model of maternal exposure to the viral mimetic polyriboinosinic-polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits in the hippocampal formation of pubescent and adult offspring. Based on the widely appreciated role of microglia in synaptic pruning, we further explored possible associations between synaptic deficits and microglia anomalies in offspring of poly(I:C)-exposed and control mothers. We found that prenatal immune activation induced an adult onset of presynaptic hippocampal deficits (as evaluated by synaptophysin and bassoon density). The early-life insult further caused postsynaptic hippocampal deficits in pubescence (as evaluated by PSD95 and SynGAP density), some of which persisted into adulthood. In contrast, prenatal immune activation did not change microglia (or astrocyte) density, nor did it alter their activation phenotypes. The prenatal manipulation did also not cause signs of persistent systemic inflammation. Despite the absence of overt glial anomalies or systemic inflammation, adult offspring exposed to prenatal immune activation displayed increased hippocampal IL-1β levels. Taken together, our findings demonstrate that age-dependent synaptic deficits and abnormal pro-inflammatory cytokine expression can occur during postnatal brain maturation in the absence of microglial anomalies or systemic inflammation.
(Copyright © 2015 Elsevier Inc. All rights reserved.)

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