Abstract
S583form ofprepulse inhibition (PPI) disruption in prenatally immunechallenged offspring, with both effects emerging only in adult butnot peri-pubertalsubjects. The causal nature ofthis relationshipis further supported by our findings that the prenatal infectioninducedPPI deficits can be normalizedby acute treatmentwith theselective DIRantagonist SCH23390 or the selective D2Rreceptorantagonist raclopride.Inconclusion, our longitudinal examination ofthe neurodevelopmental impact ofprenatal immune activation in mice revealsmultiple defects in structural and functional dopaminergic development from early fetal to adult stage of development. Ourresults highlight that dopaminergic mal-developmentin general,and following prenatal immune activation in particular, may represent a primary etiopathological mechanism in the developmentofschizophrenia and related disorders.
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