Evidence map›Paper›PMID 28860087›Full record

ArticleNeurobiology of disease2017

Pro-excitatory alterations in sodium channel activity facilitate subiculum neuron hyperexcitability in temporal lobe epilepsy.

Bryan S Barker, Aradhya Nigam, Matteo Ottolini, Ronald P Gaykema, Nicholas J Hargus, Manoj K Patel

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  7. Somatostatin-Positive Interneurons Contribute to Seizures inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  8. Resurgent Sodium Current in Neurons of the Cerebral Cortex.Frontiers in cellular neuroscience · 2021
    Article
  9. Article
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  11. Amyloid β-Induced Upregulation of NaScientific reports · 2019
    Article
  12. Article
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  14. Article
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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

6 authors at 1 institution in 1 country.

Bryan S BarkerDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia Health System, Charlottesville, VA 22908, USA.
Aradhya NigamDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Matteo OttoliniDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Ronald P GaykemaDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Nicholas J HargusDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia Health System, Charlottesville, VA 22908, USA.
Manoj K PatelDepartment of Anesthesiology, University of Virginia Health System, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia Health System, Charlottesville, VA 22908, USA. Electronic address: mkp5u@virginia.edu.
University of Virginia Health System · US

Funding

Sodium channels and neuronal excitability in chronic limbic epilepsy.R01NS075157 · NINDS · UNIVERSITY OF VIRGINIA · PI PATEL, MANOJ K · 2012 to 2016
$1.7M
NINDS NIH HHS R01 NS075157
6 · The paper itself

Abstract

Temporal lobe epilepsy (TLE) is a common form of adult epilepsy involving the limbic structures of the temporal lobe. Subiculum neurons act to provide a major output from the hippocampus and consist of a large population of endogenously bursting excitatory neurons. In TLE, subiculum neurons are largely spared, become hyperexcitable and show spontaneous epileptiform activity. The basis for this hyperexcitability is unclear, but is likely to involve alterations in the expression levels and function of various ion channels. In this study, we sought to determine the importance of sodium channel currents in facilitating neuronal hyperexcitability of subiculum neurons in the continuous hippocampal stimulation (CHS) rat model of TLE. Subiculum neurons from TLE rats were hyperexcitable, firing a higher frequency of action potentials after somatic current injection and action potential (AP) bursts after synaptic stimulation. Voltage clamp recordings revealed increases in resurgent (I

Indexed as

Action PotentialsAnimalsAnticonvulsantsDisease Models, AnimalElectric StimulationElectrodes, ImplantedEpilepsy, Temporal LobeHippocampusImmunohistochemistryMaleNeuronsNeurotransmitter AgentsPatch-Clamp TechniquesRats, Sprague-DawleySodium ChannelsStatus EpilepticusAnticonvulsantsNeurotransmitter AgentsSodium ChannelsAction potentialsElectrophysiologyNa(v)1.6Sodium channelsSubiculumTemporal lobe epilepsy

Identifiers

PMID28860087
PMCPMC5675750
OpenAlexW2753435030

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.