| Abstract | In mice, peripheral administration of the bacterial endotoxin lipopolysaccharide (LPS) activates the innate immune system, leading to deficits in hippocampus-dependent memory. D-cycloserine (DCS), a partial NMDA receptor agonist, has been shown to enhance memory consolidation in various hippocampus-dependent paradigms. Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to have a strong anti-inflammatory effect in vitro, and to restore age-related deficits in memory consolidation in a hippocampus-dependent paradigm. In our first experiment, peripherally administered DCS restored appropriate memory consolidation following systemic LPS exposure, but DCS alone did not enhance memory consolidation. In our second experiment, peripherally administered NaB failed to restore appropriate memory consolidation following systemic LPS exposure, and NaB alone did not enhance memory consolidation. In summary, post-training administration of DCS, but not NaB, rescued LPS-induced deficits in memory consolidation. |
