The effect of interleukin 1-beta (IL-1β) on memory reconsolidation is mediated by a reduction in glutamate release, calcium influx and AMPA phosphorylation. Modulation by alpha-melanocyte-stimulating hormone (α-MSH)

IVANA MACHADO; GONZALEZ PATRICIA; VILCAES AA; ROTH GA; SCIMONELLI T

Washington (DC)

Congreso; Society for Neuroscience2014; 2014

Society for Neuroscience

The immune system is an important modulator of learning, memory and neural plasticity. Interleukin 1β (IL-1β), a pro-inflammatory cytokine, affects several cognitive processes. Previous studies of our group have demonstrated that the intrahippocampal administration of IL-1β impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (-MSH). The mechanisms underlying IL-1β effect on memory reconsolidation have not been established yet. Our results demonstrate that IL-1β produce a significant decrease in the glutamate release from dorsal hippocampus synaptosomes after reactivation of the fear memory. Furthermore, experiments performed to evaluate cytosolic Ca2+ reveale that inhibition on glutamate release could be attributed to reduction in voltage-dependent Ca2+ influx. In addition, western blot analysis demonstrate a decrease in the GluR1 AMPA subunit phosphorylation by IL-1. Moreover, the intrahippocampal administration of α-MSH can modulate these effects. Our results establish a possible mechanism involved in the detrimental effect of IL-1β on memory reconsolidation and also that α-MSH may exert a beneficial modulatory role in preventing IL-1β effects.