Evidence map›Paper›PMID 28701956›Full record

ArticleFrontiers in pharmacology2017

Administration of a Histone Deacetylase Inhibitor into the Basolateral Amygdala Enhances Memory Consolidation, Delays Extinction, and Increases Hippocampal BDNF Levels.

Fernanda E Valiati, Mailton Vasconcelos, Martina Lichtenfels, Fernanda S Petry, Rosa M M de Almeida, Gilberto Schwartsmann, Nadja Schröder, Caroline B de Farias, Rafael Roesler

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  7. ACSS2-related autophagy has a dual impact on memory.Chinese neurosurgical journal · 2019
    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

9 authors at 4 institutions in 2 countries.

Fernanda E ValiatiDepartment of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Mailton VasconcelosInstitute of Psychology, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Martina LichtenfelsCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Fernanda S PetryDepartment of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Rosa M M de AlmeidaInstitute of Psychology, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Gilberto SchwartsmannCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Nadja SchröderNeurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University of Rio Grande do SulPorto Alegre, Brazil.
Caroline B de FariasCancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Rafael RoeslerDepartment of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do SulPorto Alegre, Brazil.
Universidade Federal do Rio Grande do Sul · BRUniversity of Rio Grande and Rio Grande Community College · USInstituto Federal de Educação, Ciência e Tecnologia do Rio Grande do Sul · BRPontifícia Universidade Católica do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene expression related to the formation and modification of memories is regulated epigenetically by chromatin remodeling through histone acetylation. Memory formation and extinction can be enhanced by treatment with inhibitors of histone deacetylases (HDACs). The basolateral amygdala (BLA) is a brain area critically involved in regulating memory for inhibitory avoidance (IA). However, previous studies have not examined the effects of HDAC inhibition in the amygdala on memory for IA. Here we show that infusion of an HDAC inhibitor (HDACi), trichostatin A (TSA), into the BLA, enhanced consolidation of IA memory in rats when given at 1.5, 3, or 6 h posttraining, but not when the drug was infused immediately after training. In addition, intra-BLA administration of TSA immediately after retrieval delayed extinction learning. Moreover, we show that intra-BLA TSA in rats given IA training increased the levels of brain-derived neurotrophic factor in the dorsal hippocampus, but not in the BLA itself. These findings reveal novel aspects of the regulation of fear memory by epigenetic mechanisms in the amygdala.

Indexed as

amygdalabrain-derived neurotrophic factorhippocampushistone deacetylasememory consolidationmemory extinction

Identifiers

PMID28701956
PMCPMC5487430
OpenAlexW2626069344

What OpenQuestion holds

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LicenceCC BY
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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.