The impairment on fear memory consolidation induced by IL-1beta involves MAPK p38 phosphorylation and reduction of ERK activation.

GONZALEZ P; MACHADO I; A VILCAES; ROTH G; LASAGA M; SCIMONELLI T

Cancún

Congreso; 24th Biennal Joint Meeting of the International Society for Neurochemistry (ISN) and the American Society for Neurochemistry (ASN).; 2013

International Society for Neurochemistry (ISN) and the American Society for Neurochemistry (ASN).

Pro-inflammatory cytokines and their receptors are present in the brain, specifically in the areas that are known to be involved in memory formation, such as the hippocampus. In addition, increased levels of these cytokines can produce alterations in cognitive processes. Particularly, IL-1b significantly impaired the consolidation of memories that depend on hippocampus. However, the mechanisms involved in this detrimental effect of IL-1b have not been clearly elucidated yet. Previously, we reported that IL-1b could induce a decrease in glutamate release during consolidation of contextual fear memory. Here we show that intrahippocampal administration of IL-1b increases p38 phosphorylation and that treatment with SB203580, an inhibitor of p38 activation, partially attenuates the effect of the cytokine on glutamate release. Besides, the injection of SB203580 reverses the impairment induced by IL-1b in contextual fear conditioning. We earlier demonstrated that IL-1b administration reduced ERK2 phosphorylation, a MAPK critically involved in memory consolidation and then we showed that the treatment with D-cycloserine, a partial agonist of the NMDA receptor, reverses the effect of IL-1b on ERK2 activation. Thus, in the present study we determine possible molecular mechanisms involved in the effect of IL-1b in hippocampus on fear memory consolidation.