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The age-related attenuation in long-term potentiation is associated with microglial activation

Rebecca Griffin1, Rachel Nally, Yvonne Nolan

  • 1Trinity College Institute for Neuroscience and Physiology Department, Trinity College, Dublin, Ireland.

Journal of Neurochemistry
|September 20, 2006
PubMed

Insights

Neuroinflammation, marked by increased cytokines and microglial activation, impairs long-term potentiation (LTP) in aging rats. Minocycline partially restored LTP, suggesting microglial activation contributes to age-related cognitive decline.

Area of Science:

  • Neuroscience
  • Immunology
  • Aging Research

Background:

  • Inflammatory changes are linked to brain aging and deficits in long-term potentiation (LTP).
  • Increased interleukin-1beta (IL-1beta) has been observed in aged brains, correlating with impaired LTP.
  • The exact age at which these inflammatory changes begin remains unclear.

Purpose of the Study:

  • To investigate the parallel changes in inflammation markers and LTP at different ages in rats.
  • To determine the role of microglial activation in age-related LTP deficits.

Main Methods:

  • Assessed hippocampal concentrations of proinflammatory cytokines (IL-1alpha, IL-18, IFNgamma) and microglial activation markers (CD86, CD40, ICAM) in 3-, 9-, and 15-month-old rats.
  • Measured hippocampal long-term potentiation (LTP) in rats of different ages.
  • Administered minocycline, a microglial activation inhibitor, to 15-month-old rats to assess its effect on LTP.

Main Results:

  • Older rats (9 and 15 months) exhibited increased hippocampal concentrations of IL-1alpha, IL-18, and IFNgamma.
  • Deficits in hippocampal LTP were observed in older rats, correlating with elevated cytokine levels.
  • Increased expression of microglial activation markers (CD86, CD40, ICAM) was found in older rats.
  • Administration of minocycline partially restored LTP in 15-month-old rats.

Conclusions:

  • Neuroinflammation, characterized by elevated cytokines and microglial activation, is evident in middle-aged rats.
  • Microglial activation plays a significant role in the age-related impairment of hippocampal LTP.
  • Interleukin-18 (IL-18) may be an early trigger for these neuroinflammatory changes and subsequent LTP deficits.

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