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Neonatal lipopolysaccharide induces pathological changes in parvalbumin immunoreactivity in the hippocampus of the

Trisha A Jenkins1, Michael K Harte, Gillian Stenson

  • 1Department of Psychiatry, Queen's University Belfast, Northern Ireland, UK. t.jenkins@qub.ac.uk

Behavioural Brain Research
|July 28, 2009
PubMed

Insights

Neonatal infection via lipopolysaccharide (LPS) exposure in rats caused long-term behavioral changes and reduced parvalbumin neurons in the hippocampus, potentially modeling schizophrenia risk factors.

Area of Science:

  • Neuroscience
  • Developmental Psychology
  • Psychiatry

Background:

  • Early life infection exposure is a known risk factor for schizophrenia.
  • Neonatal infection may induce lasting brain development alterations.
  • Understanding these alterations can provide insights into schizophrenia pathogenesis.

Purpose of the Study:

  • To investigate long-term behavioral and pathological effects of neonatal infection in a rat model.
  • To determine if neonatal lipopolysaccharide (LPS) administration mimics schizophrenia-related brain changes.

Main Methods:

  • Rats received lipopolysaccharide (LPS) on postnatal days 7 and 9.
  • Locomotor activity and object recognition memory were assessed at adulthood (days 35 and 70).
  • Brain tissue analysis focused on parvalbumin neuron expression in the hippocampus and prefrontal cortex.

Main Results:

  • LPS-treated rats exhibited reduced locomotor activity in adulthood.
  • A delayed deficit in object recognition memory was observed at day 70.
  • Significant reductions in parvalbumin-expressing neurons were found in the hippocampal CA1-CA3 subregions, but not the dentate gyrus or prefrontal cortex.

Conclusions:

  • Neonatal LPS exposure induces persistent behavioral impairments and specific neuropathological changes in the hippocampus.
  • These findings suggest that early-life infection can lead to lasting brain alterations relevant to schizophrenia.
  • The selective reduction of parvalbumin neurons in hippocampal subregions highlights a potential mechanism underlying infection-induced neurodevelopmental risks.

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