Evidence map›Paper›PMID 28404824›Full record

ArticleJournal of neurophysiology2017

Glycolytic inhibition by 2-deoxy-d-glucose abolishes both neuronal and network bursts in an in vitro seizure model.

Li-Rong Shao, Carl E Stafstrom

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurophysiology, 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
2.0field-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

16 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Bioenergetic Mechanisms of Seizure Control.Frontiers in cellular neuroscience · 2018
    Review
  16. Article
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

2 authors at 2 institutions in 1 country.

Li-Rong ShaoDivision of Pediatric Neurology, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland lshao5@jhmi.edu.
Carl E StafstromDivision of Pediatric Neurology, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal activity is energy demanding and coupled to cellular metabolism. In this study, we investigated the effects of glycolytic inhibition with 2-deoxy-d-glucose (2-DG) on basal membrane properties, spontaneous neuronal firing, and epileptiform network bursts in hippocampal slices. The effect of glycolytic inhibition on basal membrane properties was examined in hippocampal CA1 neurons, which are not ordinarily active spontaneously. Intracellular application of 2-DG did not significantly alter the membrane input resistance, action-potential threshold, firing pattern, or input-output relationship of these neurons compared with simultaneously recorded neighboring neurons without intracellular 2-DG. The effect of glycolytic inhibition on neuronal firing was tested in spontaneously active hippocampal neurons (CA3) when synaptic transmission was left intact or blocked with AMPA, NMDA, and GABA

Indexed as

Action PotentialsSynaptic PotentialsAnimalsAntimetabolitesCA1 Region, HippocampalCA3 Region, HippocampalDeoxyglucoseNeuronsRatsRats, Sprague-DawleySeizuresAntimetabolitesDeoxyglucosecellular excitabilityepilepsyglucose metabolismhippocampuspatch clamp

Identifiers

PMID28404824
PMCPMC5494374
OpenAlexW2607297653

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.