-Interleukin-1β-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and AMPA phosphorylation. α-melanocyte-stimulating hormone prevented these effects.

MACHADO I; GONZALEZ PV; VILCAES A; LASAGA M; SCIMONELLI T

Mar del Plata

Congreso; Reunion Anual de la Sociedad Argentina de Investigación en Neurociencias (SAN).; 2015

SAN

Interleukin-1β-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and AMPA phosphorylation. α-melanocyte-stimulating hormone prevented these effects.Ivana Machado1°, Patricia Gonzalez1°, Alejando Vilcaes2°, Mercedes Lasaga3°, Teresa Scimonelli1°1° Instituto de Farmacología Experimental Córdoba IFEC-CONICET, Facultad de Ciencias Químicas UNC,Córdoba, Argentina 2° CIQUIBIC-CONICET, Departamento de Química Biológica. Facultad de CienciasQuímicas UNC, Córdoba, Argentina 3° Instituto de Investigaciones Biomédicas INBIOMED UBACONICET,Facultad de Medicina, Buenos Aires, Argentinaivana861@hotmail.com_____________________________________________________________The immune system is an important modulator of learning, memory and neural plasticity.Interleukin 1β (IL-1β), a pro-inflammatory cytokine, significantly 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 (α-MSH). The mechanisms underlying the effect of IL-1β on memory reconsolidation have not been established yet. Our results demonstrate that IL-1β produced a significant decrease in the glutamate release from dorsal hippocampus synaptosomes after reactivation of the fear memory. Examination of the cytosolic Ca2+ using Fluo-3AM revealed that the inhibition of glutamate release could be attributed to a reduction in voltage-dependent Ca2+ influx.Also, western blot analysis demonstrated that IL-1β reduced the expression andphosphorylation of GluR1 AMPA subunit. 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.