• A M Hein, D L Stutzman, S T Bland, R M Barrientos, L R Watkins, J W Rudy, and S F Maier.
• Department of Psychology and The Center for Neuroscience, University of Colorado at Boulder, Campus Box 345, Boulder, CO 80309, USA. amy.hein@colorado.edu
• Neuroscience. 2007 Dec 19; 150 (4): 754-63.

AbstractThe intra-hippocampal administration of interleukin-1beta (IL-1beta) as well as the induction of elevated but physiological levels of IL-1beta within the hippocampus interferes with the formation of long-term memory. There is evidence suggesting that the induction of prostaglandin (PG) formation by IL-1beta is involved in impairments in working and spatial memory following IL-1beta. The present experiments extend these findings by showing that PGs are responsible for memory deficits in contextual fear conditioning that occur following IL-1beta injection into the dorsal hippocampus of Sprague-Dawley rats. Cyclooxygenase (COX) inhibition blocked the disruption in contextual fear conditioning produced by IL-1beta and COX inhibition alone also disrupted contextual memory, suggesting an inverted U-shaped relationship between PG levels and memory. In addition to demonstrating the necessity of PGs in IL-1beta-mediated memory deficits, we also show that PGs injected directly into the dorsal hippocampus are sufficient to impair context memory and significantly reduce post-conditioning levels of BDNF within the hippocampus, suggesting a possible mechanism for the memory-impairing effects of PGs.

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