Evidence map›Paper›PMID 33186637›Full record

ArticleProgress in neuro-psychopharmacology & biological psychiatry2021

Apparent reconsolidation interference without generalized amnesia.

Joaquín M Alfei, Hérnan De Gruy, Dimitri De Bundel, Laura Luyten, Tom Beckers

Abstract read
In one paragraph

Article in Progress in neuro-psychopharmacology & biological psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Joaquín M AlfeiFaculty of Psychology and Educational Sciences, KU Leuven, 3000 Leuven, Belgium; Leuven Brain Institute, KU Leuven, Leuven 3000, Belgium. Electronic address: joaquin.alfei@kuleuven.be.
Hérnan De GruyDepartment of Biology, University of Rome, 185 Rome, Italy.
Dimitri De BundelDepartment of Pharmaceutical Sciences, Research Group Experimental Pharmacology, Center for Neurosciences, Vrije Universiteit Brussel, 1050 Brussels, Belgium. Electronic address: dimitri.de.bundel@vub.be.
Laura LuytenFaculty of Psychology and Educational Sciences, KU Leuven, 3000 Leuven, Belgium; Leuven Brain Institute, KU Leuven, Leuven 3000, Belgium. Electronic address: laura.luyten@kuleuven.be.
Tom BeckersFaculty of Psychology and Educational Sciences, KU Leuven, 3000 Leuven, Belgium; Leuven Brain Institute, KU Leuven, Leuven 3000, Belgium. Electronic address: tom.beckers@kuleuven.be.

Funding

European Research Council 648176
6 · The paper itself

Abstract

Memories remain dynamic after consolidation, and when reactivated, they can be rendered vulnerable to various pharmacological agents that disrupt the later expression of memory (i.e., amnesia). Such drug-induced post-reactivation amnesia has traditionally been studied in AAA experimental designs, where a memory is initially created for a stimulus A (be it a singular cue or a context) and later reactivated and tested through exposure to the exact same stimulus. Using a contextual fear conditioning procedure in rats and midazolam as amnestic agent, we recently demonstrated that drug-induced amnesia can also be obtained when memories are reactivated through exposure to a generalization stimulus (GS, context B) and later tested for that same generalization stimulus (ABB design). However, this amnestic intervention leaves fear expression intact when at test animals are instead presented with the original training stimulus (ABA design) or a novel generalization stimulus (ABC design). The underlying mechanisms of post-reactivation memory malleability and of MDZ-induced amnesia for a generalization context remain largely unknown. Here, we evaluated whether, like typical CS-mediated (or AAA) post-reactivation amnesia, GS-mediated (ABB) post-reactivation amnesia displays key features of a destabilization-based phenomenon. We first show that ABB post-reactivation amnesia is critically dependent on prediction error at the time of memory reactivation and provide evidence for its temporally graded nature. In line with the known role of GluN2B-NMDA receptor activation in memory destabilization, we further demonstrate that pre-reactivation administration of ifenprodil, a selective antagonist of GluN2B-NMDA receptors, prevents MDZ-induced ABB amnesia. In sum, our data reveal that ABB MDZ-induced post-reactivation amnesia exhibits the hallmark features of a destabilization-dependent phenomenon. Implication of our findings for a reconsolidation-based account of post-reactivation amnesia are discussed.

Indexed as

AnimalsConditioning, ClassicalFearGeneralization, PsychologicalMaleMental RecallMidazolamRatsRats, WistarRetention, PsychologyMidazolamIfenprodilMemory generalizationMemory reconsolidationMidazolamPost-reactivation amnesia

Identifiers

PMID33186637
PMCPMC7610545

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.