Evidence map›Paper›PMID 32468095›Full record

ArticleCellular and molecular life sciences : CMLS2021

Prevention of age-associated neuronal hyperexcitability with improved learning and attention upon knockout or antagonism of LPAR2.

Caroline Fischer, Heiko Endle, Lana Schumann, Annett Wilken-Schmitz, Julia Kaiser, Susanne Gerber, Christina F Vogelaar, Mirko H H Schmidt, Robert Nitsch, Isabel Snodgrass and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

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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

13 authors at 5 institutions in 1 country.

Caroline FischerInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany.
Heiko EndleInstitute for Microscopic Anatomy and Neurobiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Lana SchumannInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany.
Annett Wilken-SchmitzInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany.
Julia KaiserInstitute for Human Genetics, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Susanne GerberInstitute for Human Genetics, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Christina F VogelaarDepartment of Neurology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Mirko H H SchmidtInstitute of Anatomy, Medical Faculty Carl Gustav Carus Technische Universität, School of Medicine, Dresden, Germany.
Robert NitschInstitute for Translational Neuroscience, Westfälische Wilhelms Universität, Münster, Germany.
Isabel SnodgrassInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany.
Dominique ThomasInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany.
Johannes Vogt *Center of Anatomy, University of Cologne, Cologne, Germany.
Irmgard Tegeder *Institute of Clinical Pharmacology, Goethe-University Frankfurt, Faculty of Medicine, Frankfurt, Germany. itegeder@hotmail.com.ORCID http://orcid.org/0000-0001-7524-8025
Goethe University Frankfurt · DEJohannes Gutenberg University Mainz · DEUniversity Hospital Carl Gustav Carus · DEUniversity of Cologne · DEUniversity of Münster · DE

Funding

Deutsche Forschungsgemeinschaft CRC1039 A03Deutsche Forschungsgemeinschaft CRC1080 A03Deutsche Forschungsgemeinschaft CRC1080 B05Deutsche Forschungsgemeinschaft SFB1193 A05
6 · The paper itself

Abstract

Recent studies suggest that synaptic lysophosphatidic acids (LPAs) augment glutamate-dependent cortical excitability and sensory information processing in mice and humans via presynaptic LPAR2 activation. Here, we studied the consequences of LPAR2 deletion or antagonism on various aspects of cognition using a set of behavioral and electrophysiological analyses. Hippocampal neuronal network activity was decreased in middle-aged LPAR2

Indexed as

AgingAnimalsBrainCalcium-Binding ProteinsChromatography, High Pressure LiquidDentate GyrusDiscriminant AnalysisEGF Family of ProteinsFemaleLiverLong-Term PotentiationMaleMaze LearningMemoryMiceMice, Inbred C57BLCalcium-Binding ProteinsEGF Family of ProteinsEgfl7 protein, mouseReceptors, Lysophosphatidic AcidCognitionHippocampal excitabilityIntelliCageLong-term potentiationLysophosphatidic acidsTouchscreen

Identifiers

PMID32468095
PMCPMC7897625
OpenAlexW3028832426

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.