CONICET | Buscador de Institutos y Recursos Humanos

NFkB is a transcription factor whose activation has been shown to be necessary forlong-term memory consolidation in several species. NFkB is activated in the nucleus of cells in aspecific temporal window during consolidation. Previous results showed that the transcriptionfactor is also present at the synapse and is activated during consolidation at different time pointsthan in the nucleus . Our work focuses on the mouse inhibitory avoidance learning paradigm. In this paradigm mice are placed on an illuminated platform with an entrance to a darkcompartment; the experimental group receives an electric shock when entering the darkcompartment. Delay on entering the compartment is evaluated 48hrs later. The behavioralcontrol group consists of mice who experience the same context as the experimental group butdo not receive an electric shock; 48hrs later this group of mice do not show a delay to enter thecompartment. Nonetheless when analyzing the activation of NFkB we found that this group ofmice has elevated activation when comparing to naïve. Furthermore, animals who receive ashock without being exposed to the platform show no delay in entering the dark compartment48hrs post training and no activation of NFkB. We argue that the mice who don?t receive theshock might perceive it as a relief (an appetitive learning situation), where they associate thecontext with a safe place and that this information may not be discriminated by the hippocampus.This appetitive memory can be impaired with an NFkB inhibitor (Sulfasalazine) injected directlyinto the hippocampus. Moreover we explore the role of the amygdala in this paradigm for boththe appetitive and aversive situations. This work aims to discuss these results and furtherinvestigate how appetitive and aversive memories are consolidated.