The impairment in memory reconsolidation induced by IL-1beta is mediated by a decrease of glutamate release and zif268 expression and alpha-MSH reversed these effects

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

Huerta Grande, Córdoba

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

SocIiedad Argentina de Investigación en Neurociencias (SAN).

The immune system plays a central role in modulating learning, memory and neural plasticity. Interleukin 1beta (IL-1b), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies of our group have demonstrated that the intrahippocampal administration of IL-1b impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (a-MSH), through activation of MC4-R. The mechanisms underlying the effect of IL-1b on memory reconsolidation have not yet been established. Thus, we examined the effect of IL-1b on Ca2-dependent glutamate release and zif268 activation during reconsolidation. Here we found that IL-1b produced  a significant decrease in glutamate release after reactivation of the fear memory and also reduced zif268 expression in the hippocampus.  The central administration of the melanocortin a-MSH can reverse the decrease of glutamate release and zif268 expression induced by IL-1b. Our results establish for the first time the possible mechanisms involved in the detrimental effect of IL-1b on memory reconsolidation and also that a-MSH may exert a benefitial modulatory role in preventing IL-1b effects