Evidence map›Paper›PMID 28067279›Full record

ArticleScientific reports2017

Impaired novelty acquisition and synaptic plasticity in congenital hyperammonemia caused by hepatic glutamine synthetase deficiency.

Aisa N Chepkova, Olga A Sergeeva, Boris Görg, Helmut L Haas, Nikolaj Klöcker, Dieter Häussinger

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Comparative analysis of adenosine 1 receptor expression and function in hippocampal and hypothalamic neurons.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  12. Instant activation of TRP channels by NHCurrent research in physiology · 2020
    Article
  13. Review
  14. Article
  15. Taurine transporter (TauT) deficiency impairs ammonia detoxification in mouse liver.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. General Pathophysiology of Astroglia.Advances in experimental medicine and biology · 2019
    Review
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.

Aisa N ChepkovaInstitute of Neural and Sensory Physiology, Heinrich Heine University, D-40225 Düsseldorf, Germany.
Olga A SergeevaInstitute of Neural and Sensory Physiology, Heinrich Heine University, D-40225 Düsseldorf, Germany.
Boris GörgDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University, D-40225 Düsseldorf, Germany.
Helmut L HaasInstitute of Neural and Sensory Physiology, Heinrich Heine University, D-40225 Düsseldorf, Germany.
Nikolaj KlöckerInstitute of Neural and Sensory Physiology, Heinrich Heine University, D-40225 Düsseldorf, Germany.
Dieter HäussingerDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University, D-40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic defects in ammonia metabolism can produce irreversible damage of the developing CNS causing an impairment of cognitive and motor functions. We investigated alterations in behavior, synaptic plasticity and gene expression in the hippocampus and dorsal striatum of transgenic mice with systemic hyperammonemia resulting from conditional knockout of hepatic glutamine synthetase (LGS-ko). These mice showed reduced exploratory activity and delayed habituation to a novel environment. Field potential recordings from LGS-ko brain slices revealed significantly reduced magnitude of electrically-induced long-term potentiation (LTP) in both CA3-CA1 hippocampal and corticostriatal synaptic transmission. Corticostriatal but not hippocampal slices from LGS-ko brains demonstrated also significant alterations in long-lasting effects evoked by pharmacological activation of glutamate receptors. Real-time RT-PCR revealed distinct patterns of dysregulated gene expression in the hippocampus and striatum of LGS-ko mice: LGS-ko hippocampus showed significantly modified expression of mRNAs for mGluR1, GluN2B subunit of NMDAR, and A1 adenosine receptors while altered expression of mRNAs for D1 dopamine receptors, the M1 cholinoreceptor and the acetylcholine-synthetizing enzyme choline-acetyltransferase was observed in LGS-ko striatum. Thus, inborn systemic hyperammonemia resulted in significant deficits in novelty acquisition and disturbed synaptic plasticity in corticostriatal and hippocampal pathways involved in learning and goal-directed behavior.

Indexed as

Exploratory BehaviorNeuronal PlasticityAnimalsBrainCerebral CortexCorpus StriatumGlutamate-Ammonia LigaseHabituation, PsychophysiologicHippocampusHyperammonemiaLiverMaleMice, KnockoutReceptors, Dopamine D2Receptors, N-Methyl-D-AspartateSynaptic TransmissionGlutamate-Ammonia LigaseReceptors, Dopamine D2Receptors, N-Methyl-D-Aspartate

Identifiers

PMID28067279
PMCPMC5220341
OpenAlexW2571206598

What OpenQuestion holds

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Read underepoch 390

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.