On the transition from reconsolidation to extinction of contextual fear memories

In this thesis we present three main studies, two regarding the transition of reconsolidation to extinction of contextual fear memories (Chapters II and III), and one on the mechanisms of reconsolidation under the synaptic tagging and capture (STC) perspective (Chapter IV). On the transition of reconsolidation to extinction, we observed a “null point” period between the parameters that induce reconsolidation and extinction of contextual fear memories, at which memory was insensitive to disruption by the amnesic agent MK-801, and some evidence for underlying STC mechanisms in the process of memory destabilization and reconsolidation. These findings reinforce and expand the hypothesis of a three-phase transition between reconsolidation and extinction of episodic-like memories and bring new insights on the different ways memory might be affected by reactivation and the mechanistic process involve

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

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

El Telegrama del Rif: El Telegrama del Rif - Año XX Número 7550 - 1921 diciembre 29 (29/12/1921)

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Papel dos receptores colinérgicos muscarínicos M4 na indução e manutenção da LTP

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