Interleukin-1beta-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and zif268 expression and alpha-melanocyte-stimulating hormone prevented these effects

MACHADO I; GONZALEZ P; VILCAEZ A; CARNIGLIA L; SCHIÖTH H; LASAGA M; SCIMONELLI T

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2015 p. 137 - 137

he immune system is an important modulator of learning, memory and neural plasticity. Interleukin 1beta (IL-1b), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies by our group have demonstrated that intrahippocampal administration of IL-1b impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (a-MSH). The mechanisms underlying the effect of IL-1b on memory reconsolidation have not yet been established. Therefore, we examined the effect of IL-1b on glutamate release, ERK phosphorylation and the activation of the transcription factor zinc finger- 268 (zif268) during reconsolidation. Our results demonstrated that IL-1b induced a significant decrease of glutamate release after reactivation of the fear memory and this effect was related to calcium concentration in hippocampal synaptosomes. IL-1b also reduced ERK phosphorylation and zif268