Following learning, a memory is fragile and undergoes a protein synthesis-dependent consolidation process in order to become stable. Established memories can again become transiently sensitive to disruption if reactivated and require another protein synthesis-dependent process, known as reconsolidation, in order to persist. Here, we show that, in the basolateral amygdala (BLA), protein synthesis is necessary for both consolidation and reconsolidation of inhibitory avoidance (IA) memory, while the expression of the transcription factor CCAAT enhancer binding protein beta (C/EBPbeta) is essential only for the reconsolidation process. Moreover, the critical roles of both protein synthesis and C/EBPbeta following IA reactivation are temporally restricted, as they are necessary only for recent but not old IA memories. These results, together with previous findings showing that in the hippocampus both protein synthesis and C/EBPbeta expression are required for consolidation but not reconsolidation of IA indicate that the stabilization process that takes place either after training or memory retrieval engages distinct neural circuits. Within these circuits, the C/EBPbeta-dependent molecular pathway appears to be differentially recruited.