Molecular mechanisms involved in the effect of IL-1beta on consolidation of fear memory

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

Huerta Grande, Córdoba

Congreso; XXVII Congreso Annual de la Sociedad Argentina de Investigación en Neurociencias (SAN).; 2012

SocIiedad Argentina de Investigación en Neurociencias (SAN).

Pro-inflammatory citokines such as IL-1beta ƒnmay affect cognitive processes by impairing synaptic plasticity through activation of MAP kinases and by inhibiting downstream mediators.  Particularly, IL-1b significantly influences consolidation of memories that depend on hippocampus. However, the mechanisms by which this inhibition occurred in vivo are not clearly established yet. We previously reported that IL-1b can induce a decrease in glutamate release during consolidation of contextual fear memory. Preliminary results showed that intrahippocampal administration of IL-1b increased p38 phosphorylation and that the treatment with SB203580, an inhibitor of p38 phosphorylation, could reverse the effect of IL-1b on glutamate release. IL-1b administration also reduced ERK2 phosphorylation, a MAPK critically involved in memory consolidation. Here, we showed that that treatment with D-cycloserine, a partial agonist of the NMDA receptor, reversed the effect of IL-1b on ERK2 phosphorylation. The evidence presented are consistent with the idea that IL-1b-induced impairment in memory consolidation could be mediated through the activation of MAPK p38 and consequently a decreased in glutamate release.