Evidence map›Paper›PMID 26441533›Full record

ArticleFrontiers in cellular neuroscience2015

Neonatal seizures alter NMDA glutamate receptor GluN2A and 3A subunit expression and function in hippocampal CA1 neurons.

Chengwen Zhou, Hongyu Sun, Peter M Klein, Frances E Jensen

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

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Chengwen ZhouDepartment of Neurology, Division of Neuroscience, Boston Children's Hospital Boston, MA, USA ; Program in Neurobiology, Harvard Medical School Boston, MA, USA.
Hongyu SunDepartment of Neurology, Division of Neuroscience, Boston Children's Hospital Boston, MA, USA ; Program in Neurobiology, Harvard Medical School Boston, MA, USA ; Department of Neurology, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.
Peter M KleinDepartment of Neurology, Division of Neuroscience, Boston Children's Hospital Boston, MA, USA.
Frances E JensenDepartment of Neurology, Division of Neuroscience, Boston Children's Hospital Boston, MA, USA ; Program in Neurobiology, Harvard Medical School Boston, MA, USA ; Department of Neurology, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.
Boston Children's Hospital · USUniversity of Pennsylvania · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI FAGIOLINI, MICHELA · 1985 to 2015
$26.2M
Understanding the Cognitive Impact of Early Life EpilepsyDP1OD003347 · OD · UNIVERSITY OF PENNSYLVANIA · PI JENSEN, FRANCES E · 2007 to 2011
$4.2M
The Epileptogenic Effect of Perinatal HypoxiaR01NS031718 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI JENSEN, FRANCES E · 1997 to 2011
$3.8M
The Epileptogenic Effect of Perinatal HypoxiaR56NS031718 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI JENSEN, FRANCES E · 2007 to 2013
$907k
NICHD NIH HHS P30 HD018655NIH HHS DP1 OD003347NINDS NIH HHS R01 NS031718NINDS NIH HHS R56 NS031718
6 · The paper itself

Abstract

Neonatal seizures are commonly caused by hypoxic and/or ischemic injury during birth and can lead to long-term epilepsy and cognitive deficits. In a rodent hypoxic seizure (HS) model, we have previously demonstrated a critical role for seizure-induced enhancement of the AMPA subtype of glutamate receptor (GluA) in epileptogenesis and cognitive consequences, in part due to GluA maturational upregulation of expression. Similarly, as the expression and function of the N-Methyl-D-aspartate (NMDA) subtype of glutamate receptor (GluN) is also developmentally controlled, we examined how early life seizures during the critical period of synaptogenesis could modify GluN development and function. In a postnatal day (P)10 rat model of neonatal seizures, we found that seizures could alter GluN2/3 subunit composition of GluNs and physiological function of synaptic GluNs. In hippocampal slices removed from rats within 48-96 h following seizures, the amplitudes of synaptic GluN-mediated evoked excitatory postsynaptic currents (eEPSCs) were elevated in CA1 pyramidal neurons. Moreover, GluN eEPSCs showed a decreased sensitivity to GluN2B selective antagonists and decreased Mg(2+) sensitivity at negative holding potentials, indicating a higher proportion of GluN2A and GluN3A subunit function, respectively. These physiological findings were accompanied by a concurrent increase in GluN2A phosphorylation and GluN3A protein. These results suggest that altered GluN function and expression could potentially contribute to future epileptogenesis following neonatal seizures, and may represent potential therapeutic targets for the blockade of future epileptogenesis in the developing brain.

Indexed as

developmentGluN receptor subunitimmature brainpost-seizuresynaptic transmission

Identifiers

PMID26441533
PMCPMC4585040
OpenAlexW1722159370

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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.