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

摘要: 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- postsynaptic deficits. Using a well-established mouse model maternal viral mimetic polyriboinosinic-polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits hippocampal formation pubescent adult offspring. Based on widely appreciated role microglia pruning, further explored possible associations between anomalies offspring poly(I:C)-exposed control mothers. We found that induced an onset presynaptic (as evaluated synaptophysin bassoon density). The early-life insult caused pubescence PSD95 SynGAP density), some which persisted into adulthood. In contrast, did not change (or astrocyte) density, nor it alter their phenotypes. manipulation signs persistent systemic inflammation. Despite absence overt glial inflammation, exposed displayed increased IL-1β levels. Taken together, our findings demonstrate age-dependent abnormal pro-inflammatory cytokine expression occur during postnatal maturation microglial