ArticleJournal of neuroinflammation2017
Functional changes in hippocampal synaptic signaling in offspring survivors of a mouse model of intrauterine inflammation.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Mild Neonatal Hypoxia Targets Synaptic Maturation, Disrupts Adult Hippocampal Learning and Memory, and Is Associated with CK2-Mediated Loss of Synaptic Calcium-Activated Potassium Channel KCNN2 Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Decreased hippocampal neurite density in late-middle-aged adults following prenatal exposure to higher levels of maternal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Decreased hippocampal neurite density in late middle-aged adults following prenatal exposure to higher levels of maternal inflammation.bioRxiv : the preprint server for biology · 2025Article
- Intrauterine Inflammation Leads to Select Sex- and Age-Specific Behavior and Molecular Differences in Mice.International journal of molecular sciences · 2022Article
- Astroglial Hemichannels and Pannexons: The Hidden Link between Maternal Inflammation and Neurological Disorders.International journal of molecular sciences · 2021Review
- Fetal Neuroprotective Strategies: Therapeutic Agents and Their Underlying Synaptic Pathways.Frontiers in synaptic neuroscience · 2021Review
- Modulating microglia activation prevents maternal immune activation induced schizophrenia-relevant behavior phenotypes via arginase 1 in the dentate gyrus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Transcutaneous Auricular Vagus Nerve Stimulation-Paired Rehabilitation for Oromotor Feeding Problems in Newborns: An Open-Label Pilot Study.Frontiers in human neuroscience · 2020Article
- Intrauterine Microbiota: Missing, or the Missing Link?Trends in neurosciences · 2019Review
- Microglia and Neonatal Brain Injury.Neuroscience · 2019Review
- The Opening of Connexin 43 Hemichannels Alters Hippocampal Astrocyte Function and Neuronal Survival in Prenatally LPS-Exposed Adult Offspring.Frontiers in cellular neuroscience · 2019Article
- In utero electroporation induces cell death and alters embryonic microglia morphology and expression signatures in the developing hypothalamus.Journal of neuroinflammation · 2018Article
- Intrauterine inflammation reduces postnatal neurogenesis in the hippocampal subgranular zone and leads to accumulation of hilar ectopic granule cells.Brain research · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent 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.
methodsAn 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.
resultsLPS 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.
conclusionsThese results offer a mechanistic explanation for the cognitive and behavioral deficits observed in survivors of preterm birth caused by intrauterine inflammation.
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