Peripheral infection and aging interact to impair hippocampal memory consolidation

We report that a peripheral injection of Escherichia coli produces both anterograde and retrograde amnesia in 24 month old, but not 3 month old rats for memories that depend on the hippocampus, that is, memory of context, contextual fear, and place learning. The anterograde effect was restricted to...

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Bibliographic Details
Published in:Neurobiology of aging 2006-05, Vol.27 (5), p.723-732
Main Authors: Barrientos, Ruth M., Higgins, Emily A., Biedenkapp, Joseph C., Sprunger, David B., Wright-Hardesty, Karli J., Watkins, Linda R., Rudy, Jerry W., Maier, Steven F.
Format: Article
Language:English
Subjects:
Acoustic Stimulation
Aging - physiology
Aging - psychology
Amnesia, Anterograde - psychology
Amnesia, Retrograde - psychology
Animals
Conditioning (Psychology) - physiology
E. coli
Escherichia coli
Escherichia coli Infections - immunology
Escherichia coli Infections - physiopathology
Escherichia coli Infections - psychology
Fear
Glial priming
Hippocampus
Hippocampus - physiopathology
Interleukin-1
Interleukin-1 - metabolism
Intraperitoneal administration
Learning
Male
Maze Learning - physiology
memory
Memory Disorders - etiology
Memory Disorders - physiopathology
Memory Disorders - psychology
Normal aging
Rats
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Summary:We report that a peripheral injection of Escherichia coli produces both anterograde and retrograde amnesia in 24 month old, but not 3 month old rats for memories that depend on the hippocampus, that is, memory of context, contextual fear, and place learning. The anterograde effect was restricted to measures of long-term memory. Short-term memory was not affected, nor did E. coli produce amnesia for auditory-cue fear conditioning. There were no age related effects on memory in vehicle-treated rats. In addition to these age-related cognitive effects of E.coli, we report that it produced a marked increased in IL-1β levels in the hippocampus, but not in parietal cortex or serum. These findings support the hypothesis that age is a vulnerability factor that increases the likelihood that an immune challenge will produce a cognitive impairment. It is possible that this cognitive vulnerability is mediated by age-related changes in the glial environment that results in an exaggerated brain pro-inflammatory response to infection.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2005.03.010