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

GONZALEZ PATRICIA; MACHADO IVANA; VILCAES A. ALEJANDRO; ROTH GERMAN A.; LASAGA MERCEDES; SCIMONELLI TERESA N.

Huerta Grande, Cordoba

Congreso; XXVII Congreso Anual de la Sociedad Argentina de Investigacion en Neurociencia (SAN); 2012

SAN

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