Evidence map›Paper›PMID 28832554›Full record

ArticleInternational journal of molecular sciences2017

Contribution of Intrinsic Lactate to Maintenance of Seizure Activity in Neocortical Slices from Patients with Temporal Lobe Epilepsy and in Rat Entorhinal Cortex.

Eskedar Ayele Angamo, Rizwan ul Haq, Jörg Rösner, Siegrun Gabriel, Zoltán Gerevich, Uwe Heinemann, Richard Kovács

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Metabolic Adaptation in Epilepsy: From Acute Response to Chronic Impairment.International journal of molecular sciences · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Bioenergetic Mechanisms of Seizure Control.Frontiers in cellular neuroscience · 2018
    Review
  11. Review
  12. 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

7 authors at 2 institutions in 2 countries.

Eskedar Ayele AngamoNeuroscience Research Center, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. eskedar.angamo@charite.de.
Rizwan ul HaqDepartment of Pharmaceutical Sciences, Abbottabad University of Sciences and Technology, Abbottabad 22500, Pakistan. rizwanhej@gmail.com.
Jörg RösnerNeuroscience Research Center, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. joerg.roesner@charite.de.
Siegrun GabrielNeuroscience Research Center, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. siegrun.gabriel@charite.de.
Zoltán GerevichInstitute for Neurophysiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. zoltan.gerevich@charite.de.
Uwe HeinemannNeuroscience Research Center, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. mozsafa@gmail.com.
Richard KovácsInstitute for Neurophysiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Charitéplatz 1, 10117 Berlin, Germany. richard.kovacs@charite.de.
Humboldt-Universität zu Berlin · DEAbbottabad University of Science and Technology · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal lactate uptake supports energy metabolism associated with synaptic signaling and recovery of extracellular ion gradients following neuronal activation. Altered expression of the monocarboxylate transporters (MCT) in temporal lobe epilepsy (TLE) hampers lactate removal into the bloodstream. The resulting increase in parenchymal lactate levels might exert both, anti- and pro-ictogen effects, by causing acidosis and by supplementing energy metabolism, respectively. Hence, we assessed the contribution of lactate to the maintenance of transmembrane potassium gradients, synaptic signaling and pathological network activity in chronic epileptic human tissue. Stimulus induced and spontaneous field potentials and extracellular potassium concentration changes (∆[K⁺]

Indexed as

Action PotentialsAnimalsEntorhinal CortexEpilepsy, Temporal LobeHumansLactic AcidNeocortexPotassiumRatsRats, WistarLactic AcidPotassiumadenosineinterictal activitylactatemesial temporal lobe epilepsymonocarboxylate transporter inhibitorsseizure

Identifiers

PMID28832554
PMCPMC5618484
OpenAlexW2749385540

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.