Evidence map›Paper›PMID 10594078›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Upregulation of GABA neurotransmission suppresses hippocampal excitability and prevents long-term potentiation in transgenic superoxide dismutase-overexpressing mice.

Y Levkovitz, E Avignone, Y Groner, M Segal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Synaptic plasticity and PDGF signaling defects underlie clinical progression in multiple sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  7. Article
  8. Article
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  10. Article
  11. Alpha5GABAA receptor activity sets the threshold for long-term potentiation and constrains hippocampus-dependent memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  12. A knock-in reporter model of Batten disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  13. Article
  14. Review
  15. Paradoxical actions of hydrogen peroxide on long-term potentiation in transgenic superoxide dismutase-1 mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  16. Absence of long-term depression in the visual cortex of glutamic Acid decarboxylase-65 knock-out mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  17. Suppression of neuronal hyperexcitability and associated delayed neuronal death by adenoviral expression of GABA(C) receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  18. Impairment of long-term potentiation and associative memory in mice that overexpress extracellular superoxide dismutase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    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

4 authors at 1 institution in 1 country.

Y LevkovitzDepartment of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel.
E Avignone
Y Groner
M Segal
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cu/Zn superoxide dismutase (SOD-1) is a key enzyme in oxygen metabolism in the brain. Overexpression of SOD-1 in transgenic (Tg) mice has been used to study the functional roles of this enzyme in oxidative stress, lipid peroxidation, and neurotoxicity. We found that Tg-SOD-1 mice are strikingly less sensitive to kainic acid-induced behavioral seizures than control mice. Furthermore, the hippocampus of Tg-SOD-1 mice was far less sensitive to local application of bicuculline, a GABA-A antagonist, than the hippocampus of control mice. GABAergic functions, expressed in extracellular paired-pulse depression, and in IPSCs recorded in dentate granular cells were enhanced in Tg-SOD-1 mice. Finally, long-term potentiation (LTP), not found in the dentate gyrus of Tg-SOD-1 mice, could be restored by local blockade of inhibition and could be blocked in control mice by injection of diazepam, which amplifies inhibition. These results indicate that constitutive elevation of SOD-1 activity exerts a major effect on neuronal excitability in the hippocampus, which, in turn, controls hippocampal ability to express LTP.

Indexed as

AnimalsElectrophysiologyEpilepsygamma-Aminobutyric AcidHippocampusHumansIn Vitro TechniquesIsoenzymesKainic AcidLong-Term PotentiationMiceMice, TransgenicNeural InhibitionPatch-Clamp TechniquesSuperoxide DismutaseSynaptic Transmissiongamma-Aminobutyric AcidIsoenzymesKainic AcidSuperoxide Dismutase

Identifiers

PMID10594078
PMCPMC6784966
OpenAlexW1916977874

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.