A new memory space is initially labile and becomes stabilized through a process of consolidation which depends on gene expression. that doubly dissociates consolidation from reconsolidation of an inhibitory avoidance memory. We then used this requirement to investigate whether reconsolidation and consolidation are involved in linking new information with reactivated memories. In contrast to what the hypothesis predicted we found that reconsolidation does not contribute to the formation of an association between new and reactivated information. Instead it recruits mechanisms similar to those underlying consolidation of a new memory. Thus linking new information to a reactivated memory is mediated by consolidation and not reconsolidation mechanisms. Introduction Memory is a dynamic process. A new memory is Zarnestra initially labile and becomes stabilized over time through a process of [1 2 This process depends on an initial phase of RNA and protein synthesis that has been characterized in several different species and with different types of memories [3-5]. Once stabilized memory is not permanently fixed and can again become labile if reactivated by recall [6-9]. Indeed memory is disrupted if several interfering occasions or pharmacological remedies including proteins synthesis inhibitors are given through the post-reactivation labile stage. Thus it’s been proposed that labile proteins synthesis-dependent stage must the reactivated memory space [6 7 9 Nevertheless the explanations why a reactivated memory space turns into labile and needs protein synthesis stay to be realized. One hypothesis proposes how the labile state from the reconsolidation procedure allows new info to be connected with founded and reactivated recollections . Even though some disagreement continues to be  many reports have demonstrated that memory reconsolidation and consolidation have distinct molecular requirements [11-13]. In particular it’s been demonstrated that both processes possess anatomically specific requirements for particular proteins and proteins synthesis generally [11 12 For instance inhibitory avoidance (IA) memory space where the animals figure out how to prevent a framework previously connected with a surprise can be disrupted by proteins synthesis inhibitors given systemically soon after reactivation recommending that like a great Ednra Zarnestra many other types of recollections IA goes through reconsolidation . Nevertheless the loan consolidation however not reconsolidation of IA memory space requires proteins synthesis as well as the Zarnestra function from the transcription element CCAAT enhancer binding proteins β (C/EBPβ) in the hippocampus [14-16] indicating that region can be differentially mixed up in two procedures. These outcomes also imply the proteins synthesis essential for the reconsolidation procedure must happen in brain areas beyond your hippocampus. Indeed in today’s study we record that IA reconsolidation however not loan consolidation needs C/EBPβ in the amygdala. Therefore the C/EBPβ necessity that differentially happens in the amygdala for reconsolidation and in the hippocampus for loan consolidation can be employed to doubly dissociate both of these processes. A paradigm that’s befitting looking into how reactivated and fresh info becomes associated is second-order fitness. Whereas a first-order traditional Pavlovian fitness involves the forming of an association between your representations from the stimuli combined during teaching (pairing between a conditioned stimulus [CS] Zarnestra with an unconditioned stimulus [US]) a second-order conditioning promotes the formation of associations between the second CS (S2) and the conditioned response elicited by the first CS (S1) [17 18 Thus the stimulus-response learning that occurs during a second-order conditioning represents the formation of an association between new (S2) and reactivated information (memory of S1-US) which makes this paradigm proper for investigating the mechanisms involved in linking new and reactivated information. Here we used the IA task modified to a second-order conditioning paradigm and the anatomically distinct C/EBPβ requirements to investigate whether as hypothesized the process of reconsolidation induced by memory reactivation is utilized to link new learning with already established and reactivated memories. Results Both the New Information and.