Treatment of fear memories: interactions between extinction and reconsolidation

Fiorenza, Natália Gindri; Sartor, Dagieli; Myskiw, Jociane C.; Izquierdo, Iván

doi:10.1590/s0001-37652011000400023

Cited by 13 publications

(7 citation statements)

References 48 publications

(81 reference statements)

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“…Reconsolidation can strengthen fear memories (57) but also provides a mechanism to reconfigure and reduce such memories (55,58,59). Extinction is often considered a form of learning (54,60,61), yet reconsolidation is a property of retrieval (61,62). These two processes can occur independently, possibly both via the amygdala (57,60,63).…”

Section: Discussionmentioning

confidence: 99%

Computerized Exposure Therapy for Spider Phobia: Effects of Cardiac Timing and Interoceptive Ability on Subjective and Behavioral Outcomes

et al. 2019

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Section: Discussionmentioning

confidence: 99%

Computerized Exposure Therapy for Spider Phobia: Effects of Cardiac Timing and Interoceptive Ability on Subjective and Behavioral Outcomes

et al. 2019

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“…The fact that performance of the distracted groups resulted in the reduction of the response naturally prompts the question of whether this was, or not, a simple case of “facilitation of extinction”. Reconsolidation and extinction have some markedly different properties: while the first seems to modify the engram in a more permanent way 11 37 38 – either reducing or increasing its intensity or quality 3 , the second usually has only a transient inhibitory effect upon memory, usually involving a new, second trace 39 40 41 42 43 44 . In extinction, fear response may return through several routes, either by the passage of time (spontaneous recovery) or after exposure to the unconditioned stimulus (reinstatement), for instance 39 45 46 47 .…”

Section: Discussionmentioning

confidence: 99%

Memory reconsolidation may be disrupted by a distractor stimulus presented during reactivation

Crestani

Boos

Haubrich

et al. 2015

Sci Rep

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Memories can be destabilized by the reexposure to the training context, and may reconsolidate into a modified engram. Reconsolidation relies on some particular molecular mechanisms involving LVGCCs and GluN2B-containing NMDARs. In this study we investigate the interference caused by the presence of a distractor - a brief, unanticipated stimulus that impair a fear memory expression - during the reactivation session, and tested the hypothesis that this disruptive effect relies on a reconsolidation process. Rats previously trained in the contextual fear conditioning (CFC) were reactivated in the presence or absence of a distractor stimulus. In the test, groups reactivated in the original context with distractor displayed a reduction of the freezing response lasting up to 20 days. To check for the involvement of destabilization / reconsolidation mechanisms, we studied the effect of systemic nimodipine (a L-VGCC blocker) or intra-CA1 ifenprodil (a selective GluN2B/NMDAR antagonist) infused right before the reactivation session. Both treatments were able to prevent the disruptive effect of distraction. Ifenprodil results also bolstered the case for hippocampus as the putative brain structure hosting this phenomenon. Our results provide some evidence in support of a behavioral, non-invasive procedure that was able to disrupt an aversive memory in a long-lasting way.

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“…The elucidation of the identity and dynamics of mechanisms involved in memory formation and reprocessing after retrieval is important not only for its theoretical value but also for the development of therapeutic strategies for pathologies related to memory dysfunctions (Lee et al, ; Fiorenza et al, ). In particular, the study of the cellular and molecular mechanisms involved in associative fear will be enlightening to contribute to the development of treatments for human phobias and post‐traumatic stress disorder.…”

Section: Discussionmentioning

confidence: 99%

Calcineurin phosphatase as a negative regulator of fear memory in hippocampus: Control on nuclear factor‐κB signaling in consolidation and reconsolidation

et al. 2014

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Protein phosphatases are important regulators of neural plasticity and memory. Some studies support that the Ca(2+) /calmodulin-dependent phosphatase calcineurin (CaN) is, on the one hand, a negative regulator of memory formation and, on the other hand, a positive regulator of memory extinction and reversal learning. However, the signaling mechanisms by which CaN exerts its action in such processes are not well understood. Previous findings support that CaN negatively regulate the nuclear factor kappaB (NF-κB) signaling pathway during extinction. Here, we have studied the role of CaN in contextual fear memory consolidation and reconsolidation in the hippocampus. We investigated the CaN control on the NF-κB signaling pathway, a key mechanism that regulates gene expression in memory processes. We found that post-training intrahippocampal administration of the CaN inhibitor FK506 enhanced memory retention one day but not two weeks after training. Accordingly, the inhibition of CaN by FK506 increased NF-κB activity in dorsal hippocampus. The administration of the NF-κB signaling pathway inhibitor sulfasalazine (SSZ) impeded the enhancing effect of FK506. In line with our findings in consolidation, FK506 administration before memory reactivation enhanced memory reconsolidation when tested one day after re-exposure to the training context. Strikingly, memory was also enhanced two weeks after training, suggesting that reinforcement during reconsolidation is more persistent than during consolidation. The coadministration of SSZ and FK506 blocked the enhancement effect in reconsolidation, suggesting that this facilitation is also dependent on the NF-κB signaling pathway. In summary, our results support a novel mechanism by which memory formation and reprocessing can be controlled by CaN regulation on NF-κB activity.

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Treatment of fear memories: interactions between extinction and reconsolidation

Cited by 13 publications

References 48 publications

Computerized Exposure Therapy for Spider Phobia: Effects of Cardiac Timing and Interoceptive Ability on Subjective and Behavioral Outcomes

Computerized Exposure Therapy for Spider Phobia: Effects of Cardiac Timing and Interoceptive Ability on Subjective and Behavioral Outcomes

Memory reconsolidation may be disrupted by a distractor stimulus presented during reactivation

Calcineurin phosphatase as a negative regulator of fear memory in hippocampus: Control on nuclear factor‐κB signaling in consolidation and reconsolidation

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