CONICET | Buscador de Institutos y Recursos Humanos

Traumatic experiences can permanent affect an individual deteriorating his quality of life. A common feature of traumatic experiences is the hypermnesia of the traumatic event and a generalization of fear. Re exposure to specific cues can be a method to teach patients to inhibit the aversive response. This is a valid line of treatment for a disorder, but it tends to be refractory to pharmacological treatments. Although in some cases appears to be effective, there is a high level of rebound of the symptoms even after initial successful treatment. This might be because the method can prevent memory expression but does not get rid of the memory itself. One potentially promising approach is to alter the original memory instead of inhibiting its expression. Recent research shows that reactivating an old memory results in a period of memory labilization that requires restorage through reconsolidation, opening a window for modification. The possibility of changing a specific memory following reactivation holds great clinical potential to improve the lives of patients that suffer from post-traumatic stress disorder. Thus, finding pharmacological compounds that can affect the reconsolidation process carry important clinical relevance. There is a long list of approved drugs to treat anxiety and post traumatic stress disorders with low efficacy. These drugs are usually administered chronically and not timed to memory reactivation and reconsolidation. We would like to explore the hypothesis that modification of the serotonergic tone during the reconsolidation process is a relevant manipulation to impair the return of unwanted traumatic memories. We evaluated the action of compounds that target the serotoninergic system in memory reconsolidation of a contextual fear memory in mice, Preliminary data points at a possible amnesic effect of a single dose of the antidepressant fluoxetine when administered within the reconsolidation window