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

Highlights • Maternal poly(I:C) challenge induces presynaptic hippocampal deficits in adult offspring. • Prenatal immune activation leads to postsynaptic hippocampal deficits in pubescence. • Hippocampal IL-1β is increased in adulthood without signs of systemic inflammation. • Synaptic deficits occu...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2016-07, Vol.55, p.25-38
Main Authors: Giovanoli, Sandra, Weber-Stadlbauer, Ulrike, Schedlowski, Manfred, Meyer, Urs, Engler, Harald
Format: Article
Language:English
Subjects:
Age Factors
Allergy and Immunology
Animals
Autism
Cytokines
Disease Models, Animal
Female
Hippocampus - immunology
Hippocampus - physiopathology
Immunologic Factors - pharmacology
Inflammation
Interleukin-1beta - metabolism
Male
Maternal immune activation
Mice
Mice, Inbred C57BL
Microglia
Microglia - immunology
Microglia - metabolism
Poly I-C - pharmacology
Poly(I:C)
Pregnancy
Prenatal Exposure Delayed Effects - immunology
Prenatal Exposure Delayed Effects - physiopathology
Psychiatry
Schizophrenia
Synapse
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Summary:Highlights • Maternal poly(I:C) challenge induces presynaptic hippocampal deficits in adult offspring. • Prenatal immune activation leads to postsynaptic hippocampal deficits in pubescence. • Hippocampal IL-1β is increased in adulthood without signs of systemic inflammation. • Synaptic deficits occur in absence of microglial anomalies.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2015.09.015