ABSTRAC FALAN 2016

Thememory consolidation impairment induced by Interleukin-1β could be associated to changesin hippocampal structural plasticity.

HerreraG1; Calfa G1; Machado I1; Lasaga M.2; Scimonelli T1 .

1IFEC-CONICET.Depto. Farmacología. Facultad de Ciencias Químicas. Universidad Nacional deCórdoba, Argentina, 2 Instituto de Investigaciones Biomédicas INBIOMEDUBA-CONICET, Facultad de Medicina, Buenos Aires, Argentina.

Pro-inflammatory cytokines can affect cognitiveprocesses, such as learning and memory. Accordingly, high levels ofinterleukin-1beta (IL-1b) in the brain could impair memory and also cytokinesparticipated in detrimental changes in cognitive functions observed during neurodegenerativediseases. Particularly, IL-1b influences the consolidation and reconsolidationof hippocampus-dependent memories.

We previously reported that administration of IL-1b indorsal hippocampus (DH) impaired contextual fear memory consolidation. We alsoshowed that IL-1b administration produced a decrease in glutamate release from DHsynaptosomes and decreased brain-derived neurotrophic factor (BDNF) expressionafter contextual fear conditioning. Considering that BDNF plays an importantrole in synaptic plasticity, in this study we evaluated if IL-1b could inducechanges in hippocampal structural plasticity. Preliminary results show that theimpairment of contextual fear memory following the IL-1b treatment wasassociated with a decrement in spine density in the DH, particularly in themature dendritic spines (mushroom and stubby) without changes in immaturedendritic spines (thin). Our data suggests that neuroinflammation interfereswith experience-dependent structural plasticity in DH.