Evidence map›Paper›PMID 24591622›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Hippocampal molecular mechanisms involved in the enhancement of fear extinction caused by exposure to novelty.

Jociane de Carvalho Myskiw, Cristiane Regina Guerino Furini, Fernando Benetti, Ivan Izquierdo

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% of its field
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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Extinction learning with social support depends on protein synthesis in prefrontal cortex but not hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Extinction of Contextual Cocaine Memories Requires CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  18. Impaired Fear Extinction Due to a Deficit in CaFrontiers in integrative neuroscience · 2017
    Article
  19. Article
  20. Major neurotransmitter systems in dorsal hippocampus and basolateral amygdala control social recognition memory.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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

4 authors at 1 institution in 1 country.

Jociane de Carvalho MyskiwNational Institute of Translational Neuroscience, National Research Council of Brazil, and Memory Center, Brain Institute, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, 90610-000, Brazil.
Cristiane Regina Guerino Furini
Fernando Benetti
Ivan Izquierdo
Pontifícia Universidade Católica do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to a novel environment enhances the extinction of contextual fear. This has been explained by tagging of the hippocampal synapses used in extinction, followed by capture of proteins from the synapses that process novelty. The effect is blocked by the inhibition of hippocampal protein synthesis following the novelty or the extinction. Here, we show that it can also be blocked by the postextinction or postnovelty intrahippocampal infusion of the NMDA receptor antagonist 2-amino-5-phosphono pentanoic acid; the inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII), autocamtide-2-related inhibitory peptide; or the blocker of L-voltage-dependent calcium channels (L-VDCCs), nifedipine. Inhibition of proteasomal protein degradation by β-lactacystin has no effect of its own on extinction or on the influence of novelty thereon but blocks the inhibitory effects of all the other substances except that of rapamycin on extinction, suggesting that their action depends on concomitant synaptic protein turnover. Thus, the tagging-and-capture mechanism through which novelty enhances fear extinction involves more molecular processes than hitherto thought: NMDA receptors, L-VDCCs, CaMKII, and synaptic protein turnover.

Indexed as

Behavior, AnimalFearAcetylcysteineAnimalsAnisomycinCalcium Channel BlockersConditioning, ClassicalExcitatory Amino Acid AntagonistsHippocampusProteasome Endopeptidase ComplexProtein Kinase InhibitorsRatsSirolimusUbiquitinAcetylcysteineAnisomycinCalcium Channel BlockersExcitatory Amino Acid AntagonistslactacystinProteasome Endopeptidase ComplexProtein Kinase InhibitorsSirolimusUbiquitinfear conditioninghippocampusmemorysynaptic plasticitysynaptic tagging and capture

Identifiers

PMID24591622
PMCPMC3970530
OpenAlexW2094256719

What OpenQuestion holds

Textmetadata
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.