Evidence map›Paper›PMID 24121115›Full record

ArticleNeurobiology of disease2014

Pacemaker GABA synaptic activity may contribute to network synchronization in pediatric cortical dysplasia.

Carlos Cepeda, Jane Y Chen, Joyce Y Wu, Robin S Fisher, Harry V Vinters, Gary W Mathern, Michael S Levine

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

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  17. GABAFrontiers in cellular neuroscience · 2020
    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

7 authors at 2 institutions in 1 country.

Carlos CepedaIntellectual and Developmental Disabilities Research Center, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA. Electronic address: ccepeda@mednet.ucla.edu.
Jane Y ChenIntellectual and Developmental Disabilities Research Center, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA.
Joyce Y WuDivision of Pediatric Neurology, Mattel Children's Hospital, David Geffen School of Medicine, University of California Los Angeles, USA.
Robin S FisherIntellectual and Developmental Disabilities Research Center, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA.
Harry V VintersDepartment of Neurology, Section of Neuropathology, David Geffen School of Medicine, University of California Los Angeles, USA.
Gary W MathernIntellectual and Developmental Disabilities Research Center, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA; Department of Neurosurgery, Mattel Children's Hospital, David Geffen School of Medicine, University of California Los Angeles, USA; Department of Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine, University of California Los Angeles, USA.
Michael S LevineIntellectual and Developmental Disabilities Research Center, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA; Department of Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine, University of California Los Angeles, USA.
University of California, Los Angeles · USNeurobehavioral Systems · US

Funding

PATHOPHYSIOLOGY OF DEVELOPING DYSPLASTIC HUMAN CORTEXR01NS038992 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CEPEDA, CARLOS T, MATHERN, GARY W. · 1999 to 2013
$3.3M
High Frequency Oscillation as a Biomarker in Childhood EpilepsyR01NS082649 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, JOYCE Y · 2013 to 2017
$1.7M
Potential Surrogate Marker of Epileptogenic CortexK23NS051637 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, JOYCE Y · 2005 to 2009
$807k
NINDS NIH HHS K23 NS051637NINDS NIH HHS NS 38992NINDS NIH HHS NS 51637NINDS NIH HHS R01 NS038992NINDS NIH HHS R01 NS082649
6 · The paper itself

Abstract

Spontaneous pacemaker γ-aminobutyric acid (GABA) receptor-mediated synaptic activity (PGA) occurs in a subset of tissue samples from pediatric epilepsy surgery patients. In the present study, based on single-cell electrophysiological recordings from 120 cases, we describe the etiologies, cell types, and primary electrophysiological features of PGA. Cells displaying PGA occurred more frequently in the areas of greatest anatomical abnormality in cases of focal cortical dysplasia (CD), often associated with hemimegalencephaly (HME), and only rarely in non-CD etiologies. PGA was characterized by rhythmic synaptic events (5-10Hz) and was observed in normal-like, dysmorphic cytomegalic, and immature pyramidal neurons. PGA was action potential-dependent, mediated by GABAA receptors, and unaffected by antagonism of glutamate receptors. We propose that PGA is a unique electrophysiological characteristic associated with CD and HME. It could represent an abnormal signal that may contribute to epileptogenesis in malformed postnatal cortex by facilitating pyramidal neuron synchrony.

Indexed as

Synaptic TransmissionAdolescentChildChild, PreschoolCortical SynchronizationEpilepsyExcitatory Postsynaptic PotentialsHumansInfantInhibitory Postsynaptic PotentialsMalformations of Cortical DevelopmentNerve NetPyramidal CellsReceptors, GABA-AReceptors, GABA-ACortical dysplasiaDevelopmentGABAPediatric epilepsySynaptic activitySynchrony

Identifiers

PMID24121115
PMCPMC3877734
OpenAlexW2092657076

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.