Evidence map›Paper›PMID 27594097›Full record

ArticlePhysiology & behavior2016

A single day of 5-azacytidine exposure during development induces neurodegeneration in neonatal mice and neurobehavioral deficits in adult mice.

Shivakumar Subbanna, Nagaraja N Nagre, Madhu Shivakumar, Balapal S Basavarajappa

Open access · greenAbstract read
In one paragraph

Article in Physiology & behavior, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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.

Shivakumar SubbannaDivision of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
Nagaraja N NagreDivision of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
Madhu ShivakumarDivision of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
Balapal S BasavarajappaDivision of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA; New York State Psychiatric Institute, New York, NY 10032, USA; Department of Psychiatry, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA. Electronic address: Basavaraj.Balapal@nki.rfmh.org.
Nathan Kline Institute for Psychiatric Research · US

Funding

Endocannabinoid Signaling in Postnatal Ethanol EffectsR01AA019443 · NIAAA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI BALAPAL, BASAVARAJ S · 2010 to 2019
$3.2M
NIAAA NIH HHS R01 AA019443
6 · The paper itself

Abstract

The present study was undertaken to evaluate the immediate and long-term effects of a single-day exposure to 5-Azacytidine (5-AzaC), a DNA methyltransferase inhibitor, on neurobehavioral abnormalities in mice. Our findings suggest that the 5-AzaC treatment significantly inhibited DNA methylation, impaired extracellular signal-regulated kinase (ERK1/2) activation and reduced expression of the activity-regulated cytoskeleton-associated protein (Arc). These events lead to the activation of caspase-3 (a marker for neurodegeneration) in several brain regions, including the hippocampus and cortex, two brain areas that are essential for memory formation and memory storage, respectively. 5-AzaC treatment of P7 mice induced significant deficits in spatial memory, social recognition, and object memory in adult mice and deficits in long-term potentiation (LTP) in adult hippocampal slices. Together, these data demonstrate that the inhibition of DNA methylation by 5-AzaC treatment in P7 mice causes neurodegeneration and impairs ERK1/2 activation and Arc protein expression in neonatal mice and induces behavioral abnormalities in adult mice. DNA methylation-mediated mechanisms appear to be necessary for the proper maturation of synaptic circuits during development, and disruption of this process by 5-AzaC could lead to abnormal cognitive function.

Indexed as

AnimalsAnimals, NewbornAzacitidineBrainBrain DiseasesDisease Models, AnimalDNA MethylationEnzyme InhibitorsFemaleGene Expression Regulation, DevelopmentalHippocampusLong-Term PotentiationMaleMaze LearningMemory DisordersMiceAzacitidineEnzyme InhibitorsPhosphopyruvate HydrataseReceptor, Cannabinoid, CB1Developing brainDNA methylationEpigeneticsMethyltransferaseNeuronal lossSynaptic plasticity

Identifiers

PMID27594097
PMCPMC5159185
OpenAlexW2510224796

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.