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

IVANA MACHADO; PATRICIA GONZALEZ; ALEJANDRO VILCAES; GERMÁN ROTH; MERCEDES LASAGA; TERESA SCIMONELLI

Huerta Grande

Congreso; XXVII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; 2012

SAN, Sociedad Argentina de neurociencias

The immune system plays a central role in modulating learning, memory and neural plasticity. Interleukin 1b (IL-1b), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies of our group have demonstrated that the intrahippocampal administration of IL-1_ 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 glutamate release and zif268 activation during reconsolidation. Here we found that IL-1b produced a significant decrease of glutamate release after reactivation of the fear memory and also reduced zif268 expression in the hippocampus. The central administration of the a-MSH can reverse both 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 beneficial modulatory role in preventing IL-1b effects.