Fear memory induced by a threatening stimulus requires the emergence of a consolidation process, dependent on new protein synthesis necessary to stabilize transient synaptic changes following acquisition. It is well known that the basolateral complex of the amygdala (BLA) participates in fear memory formation. A traumatic experience prior to learning facilitates memory formation and the generation of LTP in BLA.  The present findings support the notion that the reduced GABAergic neurotransmission in BLA induced by stress is a critical neurobiological event in such facilitating effect on fear memory. Similarly, we have shown that a similar stressful treatment prior to acquisition attenuated the vulnerability to midazolam´s disruptive effect on fear memory reconsolidation. Moreover, D-cycloserine previous to memory reactivation restored the susceptibility to this benzodiazepine ligand.  In addition, a similar stressful situation prior to memory reactivation promoted fear memory. Modulating factors implicated in such interaction are discussed.