Evidence map›Paper›PMID 23392681›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Persistent receptor activity underlies group I mGluR-mediated cellular plasticity in CA3 neuron.

Steven R Young, Shih-Chieh Chuang, Wangfa Zhao, Robert K S Wong, Riccardo Bianchi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. CRISPR-mediated activation of autism geneMolecular therapy. Nucleic acids · 2022
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  10. Review
  11. Article
  12. mGluR1 and mGluR5 Synergistically Control Cholinergic Synaptic Transmission in the Thalamic Reticular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  13. Article
  14. Extracellular glutamate exposure facilitates group I mGluR-mediated epileptogenesis in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. 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

5 authors at 1 institution in 1 country.

Steven R YoungRobert F. Furchgott Center for Neural and Behavioral Science, Department of Physiology and Pharmacology, State University of New York Downstate Medical Center, Brooklyn, New York 11203, USA.
Shih-Chieh Chuang
Wangfa Zhao
Robert K S Wong
Riccardo Bianchi
SUNY Downstate Health Sciences University · US

Funding

GLUTAMATE RECEPTORS IN EPILEPSYR01NS035481 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI WONG, ROBERT K · 1998 to 2011
$3.0M
Glutamate Receptors in EpilepsyR56NS035481 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI WONG, ROBERT K · 2008 to 2008
$390k
NINDS NIH HHS NS35481NINDS NIH HHS R01 NS035481NINDS NIH HHS R56 NS035481
6 · The paper itself

Abstract

Plastic changes in cortical activities induced by group I metabotropic glutamate receptor (mGluR) stimulation include epileptogenesis, expressed in vitro as the conversion of normal neuronal activity to persistent, prolonged synchronized (ictal) discharges. At present, the mechanism that maintains group I mGluR-induced plasticity is not known. We examined this issue using hippocampal slices from guinea pigs and mice. Agonist [(S)-3,5-dihydroxyphenylglycine (DHPG), 30-50 μm)] stimulation of group I mGluRs induces persistent prolonged synchronized (ictal-like) discharges in CA3 that are associated with three identified excitatory cellular responses-suppression of spike afterhyperpolarizations, activation of a voltage-dependent cationic current, and increase in neuronal input resistance. Persistent prolonged synchronized discharges and the underlying excitatory cellular responses maintained following induction were reversibly blocked by mGluR1 antagonists [(S)-+-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY 367385), 50, 100 μm; CPCCOEt (hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester, 100 μm], and to a lesser extent by the mGluR5 antagonist MPEP [2-methyl-6-(phenylethynyl)pyridine hydrochloride, 50 μm]. Activation of persistent cellular responses to DHPG were unaffected by tetrodotoxin (0.5-1 μm) or perfusion with low Ca(2+)(0.2 mm)-Mn(2+)(0.5 mm) media-conditions that suppress endogenous glutamate release. The pharmacological profile of the blocking action of the group I mGluR antagonist MCPG [(RS)-α-methyl-4-carboxyphenylglycine, 50-500 μm] on persistent cellular responses was different from that on cellular responses directly activated by DHPG. These data indicate that transient stimulation of group I mGluRs alters receptor properties, rendering them persistently active in the absence of applied agonist or endogenous glutamate activation. Persistent receptor activities, primarily involving mGluR1, maintain excitatory cellular responses and emergent prolonged synchronized discharges.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsCA3 Region, HippocampalGuinea PigsMaleMethoxyhydroxyphenylglycolMiceMice, KnockoutNeuronal PlasticityNeuronsOrgan Culture TechniquesReceptors, Metabotropic Glutamate3,4-dihydroxyphenylglycol6-Cyano-7-nitroquinoxaline-2,3-dionemetabotropic glutamate receptor type 1MethoxyhydroxyphenylglycolReceptors, Metabotropic Glutamate

Identifiers

PMID23392681
PMCPMC3711659
OpenAlexW1973857012

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.