Evidence map›Paper›PMID 25740117›Full record

ArticleHippocampus2015

Depression of neuronal excitability and epileptic activities by group II metabotropic glutamate receptors in the medial entorhinal cortex.

Haopeng Zhang, Nicholas I Cilz, Chuanxiu Yang, Binqi Hu, Hailong Dong, Saobo Lei

Open access · greenAbstract read
In one paragraph

Article in Hippocampus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. International journal of molecular sciences · 2022
    Review
  5. Article
  6. 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

6 authors at 2 institutions in 2 countries.

Haopeng ZhangDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
Nicholas I CilzDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
Chuanxiu YangDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
Binqi HuDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
Hailong DongDepartment of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.
Saobo LeiDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
University of North Dakota · USXijing Hospital · CN

Funding

Roles and mechanisms of neurotensin in learning and memoryR01MH082881 · NIMH · UNIVERSITY OF NORTH DAKOTA · PI LEI, SAOBO · 2008 to 2015
$2.5M
NIMH NIH HHS R01 MH082881NIMH NIH HHS R01MH082881
6 · The paper itself

Abstract

Whereas the ionotropic glutamate receptors are the major mediator in glutamatergic transmission, the metabotropic glutamate receptors (mGluRs) usually play a modulatory role. Whereas the entorhinal cortex (EC) is an essential structure involved in the generation and propagation of epilepsy, the roles and mechanisms of mGluRs in epilepsy in the EC have not been determined. Here, we studied the effects of activation of group II metabotropic glutamate receptors (mGluRs II) on epileptiform activity induced by picrotoxin or deprivation of extracellular Mg2+ and neuronal excitability in the medial EC. We found that activation of mGluRs II by application of the selective agonist, LY354740, exerted robust inhibition on epileptiform activity. LY354740 hyperpolarized entorhinal neurons via activation of a K+ conductance and inhibition of a Na+ -permeable channel. LY354740-induced hyperpolarization was G protein-dependent, but independent of adenylyl cyclase and protein kinase A. However, the function of Gβγ was involved in mGluRs II-mediated depression of both neuronal excitability and epileptiform activity. Our results provide a novel cellular mechanism to explain the antiepileptic effects of mGluRs II in the treatment of epilepsy.

Indexed as

AnimalsBridged Bicyclo CompoundsDisease Models, AnimalEntorhinal CortexEpilepsyExcitatory Amino Acid AgonistsMagnesiumRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateSynaptic PotentialsBridged Bicyclo CompoundseglumetadExcitatory Amino Acid AgonistsMagnesiummetabotropic glutamate receptor 2Receptors, Metabotropic Glutamateaction potentialcortexepilepsyglutamatehippocampushyperpolarizationK+ channelssynaptic transmission

Identifiers

PMID25740117
PMCPMC12317764
OpenAlexW2127573978

What OpenQuestion holds

Textmetadata
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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.