Evidence map›Paper›PMID 30607810›Full record

ArticleCellular and molecular neurobiology2019

Transient Switching of NMDA-Dependent Long-Term Synaptic Potentiation in CA3-CA1 Hippocampal Synapses to mGluR

Tatyana Y Postnikova, Alina M Trofimova, Julia L Ergina, Olga E Zubareva, Sergey V Kalemenev, Aleksey V Zaitsev

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Altered Excitation-Inhibition Balance and mGluRInternational journal of molecular sciences · 2026
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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

6 authors at 1 institution in 1 country.

Tatyana Y PostnikovaLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia.
Alina M TrofimovaLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia.
Julia L ErginaLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia.
Olga E ZubarevaLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia.
Sergey V KalemenevLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia.
Aleksey V ZaitsevLaboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), Saint Petersburg, Russia. aleksey_zaitsev@mail.ru.ORCID http://orcid.org/0000-0002-4503-0647
Institute of Evolutionary Physiology and Biochemistry · RU

Funding

Russian Foundation for Basic Research 17-00-00408Russian Science Foundation 16-15-10202
6 · The paper itself

Abstract

The mechanisms of impairment in long-term potentiation after status epilepticus (SE) remain unclear. We investigated the properties of LTP induced by theta-burst stimulation in hippocampal slices of rats 3 h and 1, 3, and 7 days after SE. Seizures were induced in 3-week old rats by a single injection of pentylenetetrazole (PTZ). Only animals with generalized seizures lasting more than 30 min were included in the experiments. The results revealed that LTP was strongly attenuated in the CA1 hippocampal area after PTZ-induced SE as compared with that in control animals. Saturation of synaptic responses following epileptic activity does not explain weakening of LTP because neither the quantal size of the excitatory responses nor the slopes of the input-output curves for field excitatory postsynaptic potentials changed in the post-SE rats. After PTZ-induced SE, NMDA-dependent LTP was suppressed, and LTP transiently switched to the mGluR

Indexed as

Long-Term PotentiationAnimalsCA1 Region, HippocampalCA3 Region, HippocampalExcitatory Postsynaptic PotentialsMaze LearningN-MethylaspartatePentylenetetrazoleRats, WistarReceptors, AMPAReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateSeizuresSpatial MemorySynapsesmetabotropic glutamate receptor type 1N-MethylaspartatePentylenetetrazoleReceptors, AMPAReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateAnimal modelEpilepsyGroup I mGlu receptorLong-term potentiationmGluR-dependent plasticityNMDA receptor

Identifiers

PMID30607810
PMCPMC11469857
OpenAlexW2907593459

What OpenQuestion holds

Textmetadata
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.