Peripheral infection and aging interact to impair hippocampal memory consolidation

• 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
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2005.03.010

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.