A fear memory can be disrupted by the exposure to an appetitive stimulus after reactivation: Role of NR2b receptors in the Basolateral Amygdala

FERRER, R I; GIACHERO, M; BUENO, A M; MOLINA, V A

Huerta Grande, Córdoba

Congreso; XXVIII Congreso annual de la Sociedad Argentina de Investigación en Neurociencias & Reunión Satélite / Neurobiología del comportamiento: ?Neuroetología y Neurobiología de la memoria en el Cono Sur?; 2013

Sociedad Argentina de Neurociencias

To date, there is no experimental data regarding the possibility that a fear memory can be influenced by a rewarding experience after reactivation. To explore this, animals were habituated to voluntary sucrose consumption (SUC) and later on subjected to a contextual fear conditioning procedure. Reactivation conditions to destabilize the fear memory were determined by systemic administration of Midazolam, a GABA-A ligand agent. Various SUC concentrations (10, 20 and 30 %) were tested to determine which one induces the highest voluntary consumption. After establishing these parameters, a series of experiments explored if the original fear memory could be influenced by the appetitive stimulus after its reactivation. Experiment 1 confirmed this hypothesis: the fear memory was disrupted by the SUC experience only if such trace was destabilized after retrieval, as demonstrated in a 24 h post reactivation test. Experiment 2 revealed that this effect is absent if SAC consumption takes place outside the reconsolidation window (6 h after retrieval). Experiment 3 showed that this effect is dependent on SAC concentration and that SUC-induced memory disruption is persistent. Experiment 4 showed that intra-Basolateral Amygdala infusion of the NR2b antagonist Ifenprodil, prior to memory reactivation, blocked the impairing effects of SUC on fear memory. Our data suggests that an appetitive experience, following reactivation-induced destabilization, can interfere with a fear memory.