Functional changes in hippocampal synaptic signaling in offspring survivors of a mouse model of intrauterine inflammation

Melissa H. Kelley, Wendy W. Wu, Jun Lei, Michael McLane, Han Xie, Kyle D. Hart, Leonardo Pereira, Irina Burd, James Maylie

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Background: Recent evidence suggests that exposure to intrauterine inflammation causes acute fetal brain injury and is linked to a spectrum of neurobehavioral disorders. In a rodent model of intrauterine inflammation induced by lipopolysaccharide (LPS) exposure in utero, activated microglia can be detected in the hippocampus of offspring survivors, as late as 60 days postnatal (DPN). Given that the hippocampus is important for learning and memory, these results suggest that in utero inflammation underlies long-term cognitive deficits observed in children/survivors. Methods: An established mouse model of LPS-induced intrauterine inflammation was used to study hippocampal function from offspring at 44-59 DPN. Microgliosis was examined at 45 DPN. Extracellular field recordings of synaptic transmission were performed on acute hippocampal slices. Results: LPS offspring mice displayed persistent microglial activation and increased CA3-CA1 excitatory synaptic strength, which can be explained in part by an increase in the probability of glutamate release, and reduced long-term synaptic potentiation compared to control mice. Conclusions: These results offer a mechanistic explanation for the cognitive and behavioral deficits observed in survivors of preterm birth caused by intrauterine inflammation.

Original languageEnglish (US)
Article number180
JournalJournal of Neuroinflammation
Issue number1
StatePublished - Sep 5 2017


  • Hippocampus
  • Intrauterine inflammation
  • Long-term synaptic potentiation
  • Synaptic transmission

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience


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