Evidence map›Paper›PMID 25632125›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Hyperexcitability of rat thalamocortical networks after exposure to general anesthesia during brain development.

Michael R DiGruccio, Srdjan Joksimovic, Pavle M Joksovic, Nadia Lunardi, Reza Salajegheh, Vesna Jevtovic-Todorovic, Mark P Beenhakker, Howard P Goodkin, Slobodan M Todorovic

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  19. Is a β cell a β cell?Current opinion in endocrinology, diabetes, and obesity · 2017
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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

9 authors at 3 institutions in 3 countries.

Michael R DiGruccioDepartment of Anesthesiology, Neuroscience Graduate Program.
Srdjan JoksimovicDepartment of Anesthesiology, Department of Pharmacology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia.
Pavle M JoksovicDepartment of Anesthesiology.
Nadia LunardiDepartment of Anesthesiology.
Reza SalajeghehDepartment of Anesthesiology.
Vesna Jevtovic-TodorovicDepartment of Anesthesiology, Neuroscience Graduate Program, Neuroscience.
Mark P BeenhakkerNeuroscience Graduate Program, Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, and.
Howard P GoodkinNeuroscience Graduate Program, Departments of Neurology, Neuroscience, Pediatrics, and.ORCID http://orcid.org/0000-0003-0528-4949
Slobodan M TodorovicDepartment of Anesthesiology, Neuroscience Graduate Program, Neuroscience, st9d@virginia.edu.
Bioscience Research · USSociety for Neuroscience · USUniversity of Belgrade · RS

Funding

Anesthesia-induced developmental neurodegenerationR01HD044517 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI JEVTOVIC-TODOROVIC, VESNA · 2005 to 2014
$3.0M
In vivo imaging of thalamocortical excitability during anesthesiaR01GM102525 · NIGMS · UNIVERSITY OF VIRGINIA · PI TODOROVIC, SLOBODAN M. · 2014 to 2020
$2.0M
Mechanisms compromising GABAergic synaptic transmission during status epiletpicusR01NS067439 · NINDS · UNIVERSITY OF VIRGINIA · PI GOODKIN, HOWARD P · 2009 to 2013
$1.6M
NICHD NIH HHS HD-044517NICHD NIH HHS R01 HD044517NIGMS NIH HHS GM-102525NIGMS NIH HHS R01 GM102525NINDS NIH HHS NS-067439NINDS NIH HHS R01 NS067439
6 · The paper itself

Abstract

Prevailing literature supports the idea that common general anesthetics (GAs) cause long-term cognitive changes and neurodegeneration in the developing mammalian brain, especially in the thalamus. However, the possible role of GAs in modifying ion channels that control neuronal excitability has not been taken into consideration. Here we show that rats exposed to GAs at postnatal day 7 display a lasting reduction in inhibitory synaptic transmission, an increase in excitatory synaptic transmission, and concomitant increase in the amplitude of T-type calcium currents (T-currents) in neurons of the nucleus reticularis thalami (nRT). Collectively, this plasticity of ionic currents leads to increased action potential firing in vitro and increased strength of pharmacologically induced spike and wave discharges in vivo. Selective blockade of T-currents reversed neuronal hyperexcitability in vitro and in vivo. We conclude that drugs that regulate thalamic excitability may improve the safety of GAs used during early brain development.

Indexed as

Anesthesia, GeneralCerebral CortexThalamus4-ButyrolactoneAction PotentialsAnimalsAnimals, NewbornBenzamidesCalcium Channel BlockersDose-Response Relationship, DrugEpilepsyEvoked Potentials, SomatosensoryExcitatory Postsynaptic PotentialsFemaleInhibitory Postsynaptic PotentialsIn Vitro Techniques3,5-dichloro-N-(1-(2,2-dimethyltetrahydropyran-4-ylmethyl)-4-fluoropiperidin-4-ylmethyl)benzamide4-ButyrolactoneBenzamidesCalcium Channel BlockersPiperidinesanesthesiaGABAA receptorglutamatelow-voltage-activatedT-channelsthalamus

Identifiers

PMID25632125
PMCPMC4308595
OpenAlexW2029992003

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.