Evidence map›Paper›PMID 30918308›Full record

ArticleScientific reports2019

Histone deacetylase inhibitors restore normal hippocampal synaptic plasticity and seizure threshold in a mouse model of Tuberous Sclerosis Complex.

Trina Basu, Kenneth J O'Riordan, Barry A Schoenike, Nadia N Khan, Eli P Wallace, Genesis Rodriguez, Rama K Maganti, Avtar Roopra

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Trina BasuDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Kenneth J O'RiordanDepartment of Neurology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Barry A SchoenikeDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Nadia N KhanDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Eli P WallaceDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Genesis RodriguezDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.ORCID http://orcid.org/0000-0001-5159-533X
Rama K MagantiDepartment of Neurology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Avtar RoopraDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin, United States of America. asroopra@wisc.edu.
University of Wisconsin–Madison · USUniversity of Wisconsin System · US

Funding

Probing the Protective Role of EZH2 in EpilepsyR01NS108756 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI DINGLEDINE, RAYMOND J, ROOPRA, AVTAR S · 2019 to 2023
$2.5M
Exploring a Potential Role for Epigenetics in Tuberous Sclerosis ComplexR21NS095187 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI ROOPRA, AVTAR S · 2016 to 2017
$408k
NINDS NIH HHS R01 NS108756NINDS NIH HHS R21 NS095187
6 · The paper itself

Abstract

Abnormal synaptic plasticity has been implicated in several neurological disorders including epilepsy, dementia and Autism Spectrum Disorder (ASD). Tuberous Sclerosis Complex (TSC) is an autosomal dominant genetic disorder that manifests with seizures, autism, and cognitive deficits. The abnormal intracellular signaling underlying TSC has been the focus of many studies. However, nothing is known about the role of histone modifications in contributing to the neurological manifestations in TSC. Dynamic regulation of chromatin structure via post translational modification of histone tails has been implicated in learning, memory and synaptic plasticity. Histone acetylation and associated gene activation plays a key role in plasticity and so we asked whether histone acetylation might be dysregulated in TSC. In this study, we report a general reduction in hippocampal histone H3 acetylation levels in a mouse model of TSC2. Pharmacological inhibition of Histone Deacetylase (HDAC) activity restores histone H3 acetylation levels and ameliorates the aberrant plasticity in TSC2

Indexed as

AcetylationAnimalsBlotting, WesternElectrophysiologyHistone Deacetylase InhibitorsHistone DeacetylasesMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLSeizuresSignal TransductionTuberous SclerosisTuberous Sclerosis Complex 2 ProteinHistone Deacetylase InhibitorsHistone DeacetylasesMechanistic Target of Rapamycin Complex 1Tsc2 protein, mouseTuberous Sclerosis Complex 2 Protein

Identifiers

PMID30918308
PMCPMC6437206
OpenAlexW2923166067

What OpenQuestion holds

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Registered trials

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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.