Evidence map›Paper›PMID 19531374›Full record

ArticleNeuroscience2009

Histone deactylase inhibition combined with behavioral therapy enhances learning and memory following traumatic brain injury.

P K Dash, S A Orsi, A N Moore

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
7.4field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 138 citations in OpenAlex.

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  15. Microbiota-Gut-Brain Axis Regulation of Adult Hippocampal Neurogenesis.Brain plasticity (Amsterdam, Netherlands) · 2022
    Review
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14 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

P K DashDepartment of Neurobiology and Anatomy, The University of Texas Medical School, Houston, TX 77225, USA. p.dash@uth.tmc.edu
S A Orsi
A N Moore
The University of Texas at Austin · US

Funding

Working memory deficits following brain traumaR01NS049160 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2005 to 2009
$1.8M
Tuberous sclerosis complex in memory formationR01NS053588 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2007 to 2011
$1.6M
Prefrontal cortex and memory storageR01MH072933 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2006 to 2010
$1.5M
NIMH NIH HHS MH072933NIMH NIH HHS R01 MH072933NINDS NIH HHS NS049160NINDS NIH HHS NS053588NINDS NIH HHS R01 NS049160NINDS NIH HHS R01 NS053588
6 · The paper itself

Abstract

Traumatic brain injury (TBI) induces a number of pathological events ranging from neuronal degeneration and tissue loss to impaired neuronal plasticity and neurochemical dysregulation. In rodents, exposure of brain-injured animals to environmental enrichment has been shown to be an effective means of enhancing learning and memory post-injury. Recently, it has been discovered that environmental enrichment may enhance neuronal plasticity through epigenetic changes that involve enhanced histone acetylation, a property that can be mimicked by the use of histone deactylase (HDAC) inhibitors. We therefore evaluated the consequences of the HDAC inhibitor sodium butyrate on the learning and memory of brain-injured mice. In contrast to a previous report using a mouse neurodegeneration model, sodium butyrate (1.2 g/kg daily for four weeks) did not improve learning and memory when tested after the completion of the drug treatment paradigm. In addition, sodium butyrate administration during the reported period of neurodegeneration (days 0-5) also offered no benefit. However, when administered concurrently with training in the Morris water maze task (beginning on day 14 post-injury), sodium butyrate improved learning and memory in brain-injured mice. Interestingly, when these mice were subsequently tested in an associative fear conditioning task, an improvement was observed. Taken together, our findings indicate that HDAC inhibition may mimic some of the cognitive improvements seen following enriched environment exposure, and that the improvement is observed when the treatment is carried out current with behavioral testing.

Indexed as

AnimalsAvoidance LearningBehavior TherapyBrainBrain InjuriesButyratesConditioning, PsychologicalDisease Models, AnimalEnvironment, ControlledEpigenesis, GeneticHistone Deacetylase 1Learning DisabilitiesMaleMaze LearningMemory DisordersMiceButyratesHdac1 protein, mouseHistone Deacetylase 1

Identifiers

PMID19531374
PMCPMC4217276
OpenAlexW1981559730

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.