Evidence map›Paper›PMID 29915867›Full record

ArticleBrain structure & function2018

Ablation of the presynaptic organizer Bassoon in excitatory neurons retards dentate gyrus maturation and enhances learning performance.

Anil Annamneedi, Gürsel Caliskan, Sabrina Müller, Dirk Montag, Eike Budinger, Frank Angenstein, Anna Fejtova, Wolfgang Tischmeyer, Eckart D Gundelfinger, Oliver Stork

Open access · hybridAbstract read
In one paragraph

Article in Brain structure & function, 2018. 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
1.3field-weighted citation impact, top 23% 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, 30 citations in OpenAlex.

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  11. Organization of Presynaptic Autophagy-Related Processes.Frontiers in synaptic neuroscience · 2022
    Review
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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

10 authors at 3 institutions in 1 country.

Anil AnnamneediDepartment of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Gürsel CaliskanDepartment of Genetics and Molecular Neurobiology, Institute of Biology, Otto-von-Guericke-University, Magdeburg, Germany.
Sabrina MüllerDepartment of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Dirk MontagNeurogenetics Laboratory, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Eike BudingerDepartment of Systems Physiology of Learning, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Frank AngensteinSpecial Laboratory Noninvasive Brain Imaging, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Anna FejtovaDepartment of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Wolfgang TischmeyerCenter for Behavioral Brain Sciences (CBBS), Magdeburg, Germany.
Eckart D GundelfingerDepartment of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Magdeburg, Germany.
Oliver StorkDepartment of Genetics and Molecular Neurobiology, Institute of Biology, Otto-von-Guericke-University, Magdeburg, Germany. oliver.stork@ovgu.de.
Leibniz Institute for Neurobiology · DECenter for Behavioral Brain Sciences · DEGerman Center for Neurodegenerative Diseases · DE

Funding

Deutsche Forschungsgemeinschaft CRC 779-Neurobiology of Motivated Behavior project A06Deutsche Forschungsgemeinschaft CRC 779-Neurobiology of Motivated Behavior project B05Deutsche Forschungsgemeinschaft CRC 779-Neurobiology of Motivated Behavior project B09Leibniz-Gemeinschaft LGS SynaptogeneticsLeibniz-Gemeinschaft LGS SynaptoGenetics
6 · The paper itself

Abstract

Bassoon is a large scaffolding protein of the presynaptic active zone involved in the development of presynaptic terminals and in the regulation of neurotransmitter release at both excitatory and inhibitory brain synapses. Mice with constitutive ablation of the Bassoon (Bsn) gene display impaired presynaptic function, show sensory deficits and develop severe seizures. To specifically study the role of Bassoon at excitatory forebrain synapses and its relevance for control of behavior, we generated conditional knockout (Bsn cKO) mice by gene ablation through an Emx1 promoter-driven Cre recombinase. In these animals, we confirm selective loss of Bassoon from glutamatergic neurons of the forebrain. Behavioral assessment revealed that, in comparison to wild-type littermates, Bsn cKO mice display selectively enhanced contextual fear memory and increased novelty preference in a spatial discrimination/pattern separation task. These changes are accompanied by an augmentation of baseline synaptic transmission at medial perforant path to dentate gyrus (DG) synapses, as indicated by increased ratios of field excitatory postsynaptic potential slope to fiber volley amplitude. At the structural level, an increased complexity of apical dendrites of DG granule cells can be detected in Bsn cKO mice. In addition, alterations in the expression of cellular maturation markers and a lack of age-dependent decrease in excitability between juvenile and adult Bsn cKO mice are observed. Our data suggest that expression of Bassoon in excitatory forebrain neurons is required for the normal maturation of the DG and important for spatial and contextual memory.

Indexed as

AnimalsBehavioral ResearchCerebral CortexDentate GyrusFearHippocampusMagnetic Resonance ImagingMaleMiceMice, KnockoutNerve Tissue ProteinsNeurogenesisNeuronal PlasticityNeuronsPresynaptic TerminalsSpatial MemoryBsn protein, mouseNerve Tissue ProteinsBassoonContextual fear memoryImmature DGKnockout miceNeurogenesisSpatial memory

Identifiers

PMID29915867
PMCPMC6132633
OpenAlexW2809656951

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.