The recall of a consolidated memory by the presentation of the conditioned stimulus goes to a labile state followed by a new process of stabilization protein synthesis dependent ?reconsolidation - (Nader et al 2000, Dudai 2006)

In this way, the process of labilization-reconsolidation presents a temporal course that is vulnerable to interfering agents. However, a negative emotional state, generated by a stressing event exposure, limits the occurrence of such process and induces a resistance of the memory trace to the amnesic effect of the interfering agents during reconsolidation (Bustos et al. 2010, Ortiz et al. 2015).

The basolateral Amygdala complex (BLA) presents key role on emotional information processing as well as in the formation and recall of a contextual fear memory. In the same way, experimental evidences grant the dorsal Hippocampus (DH) the contextual representation of such fear memory thru functional interconnections between both areas.

The majority of the excitatory contacts between neurons reside on dendritic spines (Yuste and Denk 1995). Different experimental evidences have shown that the substrate for the storage of long-term memories, including contextual fear memories underlie on an appropriate structural plasticity in the form of changes in spine density, in critical brain regions following learning (Kandel 2001; Restivo et al 2009).

The aim of the present work was to characterize the modulator role of BLA on the hippocampal structural plasticity after the reactivation of such memory.