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Microglia and memory: modulation by early-life infection.

Lauren L Williamson1, Paige W Sholar, Rishi S Mistry

  • 1Department of Psychology and Neuroscience, Duke University, Durham, North Carolina 27708, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|October 28, 2011
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Summary

Neonatal infection sensitizes brain microglia, leading to increased interleukin-1β (IL-1β) during learning. This early-life event impacts adult memory function, highlighting microglial role in cognitive deficits.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cognitive Science

Background:

  • Interleukin-1β (IL-1β), a proinflammatory cytokine, is crucial for hippocampus-dependent memory but elevated levels impair cognition and are linked to neurodegeneration.
  • The cellular origin of IL-1β during learning and factors contributing to its dysregulation in the hippocampus (HP) remain unclear.
  • Neonatal bacterial infection in rats causes long-term HP-dependent memory deficits, particularly when reactivated by a secondary immune challenge (lipopolysaccharide, LPS) during adulthood.

Purpose of the Study:

  • To identify the specific cell type responsible for producing IL-1β during normal hippocampus-dependent learning.
  • To investigate how early-life infection influences the cellular source of IL-1β and its contribution to memory impairment.
  • To elucidate the mechanism by which early-life events permanently alter cytokine activity in the brain's immune cells.

Main Methods:

  • Utilized CD11b(+) cell enrichment to isolate and analyze cytokine production in the hippocampus.
  • Assessed ex vivo IL-1β production from CD11b(+) cells in neonatally infected (NI) rats compared to controls.
  • Investigated the role of microglial activation during learning in memory performance in NI rats, with and without LPS challenge.

Main Results:

  • Demonstrated that CD11b(+) enriched cells are the primary source of IL-1β during normal hippocampus-dependent learning.
  • Found that CD11b(+) cells from NI rats exhibit functional sensitization, producing exaggerated IL-1β ex vivo.
  • Showed that preventing microglial activation during learning rescues memory deficits in NI rats, even after an LPS challenge.

Conclusions:

  • Early-life infections can induce lasting changes in brain microglial function, altering their response during learning.
  • Microglia are the key cellular mediators of IL-1β dysregulation in the hippocampus following early-life adversity.
  • Modulating microglial activity during learning presents a potential therapeutic target for preventing cognitive deficits associated with early-life insults.