Evidence map›Paper›PMID 34948152›Full record

ArticleInternational journal of molecular sciences2021

Impairments of Long-Term Synaptic Plasticity in the Hippocampus of Young Rats during the Latent Phase of the Lithium-Pilocarpine Model of Temporal Lobe Epilepsy.

Tatyana Y Postnikova, Georgy P Diespirov, Dmitry V Amakhin, Elizaveta N Vylekzhanina, Elena B Soboleva, Aleksey V Zaitsev

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  7. Article
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  9. Article
  10. Article
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  12. Article
  13. Molecular and Cellular Mechanisms of Epilepsy.International journal of molecular sciences · 2023
    Article
  14. Article
  15. Beneficial Effects of ProbioticInternational journal of molecular sciences · 2023
    Article
  16. The JAK-STAT Signaling Pathway in Epilepsy.Current neuropharmacology · 2023
    Review
  17. Assessing seizure liabilityFrontiers in cellular neuroscience · 2023
    Article
  18. Review
  19. Article
  20. 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 1 institution in 1 country.

Tatyana Y PostnikovaSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.ORCID 0000-0002-7049-4478
Georgy P DiespirovSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.
Dmitry V AmakhinSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.
Elizaveta N VylekzhaninaSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.
Elena B SobolevaSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.
Aleksey V ZaitsevSechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.ORCID 0000-0002-4503-0647
Institute of Evolutionary Physiology and Biochemistry · RU

Funding

Russian Science Foundation 21-15-00430
6 · The paper itself

Abstract

Status epilepticus (SE) causes persistent abnormalities in the functioning of neuronal networks, often resulting in worsening epileptic seizures. Many details of cellular and molecular mechanisms of seizure-induced changes are still unknown. The lithium-pilocarpine model of epilepsy in rats reproduces many features of human temporal lobe epilepsy. In this work, using the lithium-pilocarpine model in three-week-old rats, we examined the morphological and electrophysiological changes in the hippocampus within a week following pilocarpine-induced seizures. We found that almost a third of the neurons in the hippocampus and dentate gyrus died on the first day, but this was not accompanied by impaired synaptic plasticity at that time. A diminished long-term potentiation (LTP) was observed following three days, and the negative effect of SE on plasticity increased one week later, being accompanied by astrogliosis. The attenuation of LTP was caused by the weakening of N-methyl-D-aspartate receptor (NMDAR)-dependent signaling. NMDAR-current was more than two-fold weaker during high-frequency stimulation in the post-SE rats than in the control group. Application of glial transmitter D-serine, a coagonist of NMDARs, allows the enhancement of the NMDAR-dependent current and the restoration of LTP. These results suggest that the disorder of neuron-astrocyte interactions plays a critical role in the impairment of synaptic plasticity.

Indexed as

AnimalsDisease Models, AnimalEpilepsy, Temporal LobeHippocampusLithiumLong-Term PotentiationMalePilocarpineRatsRats, WistarLithiumPilocarpineastrocyteD-serineexcitatory postsynaptic currentfield potentialglial fibrillary acidic proteinhippocampuslong-term potentiationNMDAtemporal lobe epilepsy

Identifiers

PMID34948152
PMCPMC8705146
OpenAlexW4200435036

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.