Evidence map›Paper›PMID 19759304›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

The role of granulocyte-colony stimulating factor (G-CSF) in the healthy brain: a characterization of G-CSF-deficient mice.

Kai Diederich, Sevgi Sevimli, Henrike Dörr, Evelin Kösters, Maike Hoppen, Lars Lewejohann, Rainer Klocke, Jens Minnerup, Stefan Knecht, Sigrid Nikol and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 84 citations in OpenAlex.

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  14. Granulocyte Colony Stimulating Factor Enhances Reward Learning through Potentiation of Mesolimbic Dopamine System Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

15 authors at 7 institutions in 3 countries.

Kai DiederichDepartment of Neurology, University of Muenster, 48149 Muenster, Germany. kai.diederich@uni-muenster.de
Sevgi Sevimli
Henrike Dörr
Evelin Kösters
Maike Hoppen
Lars Lewejohann
Rainer Klocke
Jens Minnerup
Stefan Knecht
Sigrid Nikol
Norbert Sachser
Armin Schneider
Ali Gorji
Clemens Sommer
Wolf-Rüdiger Schäbitz
Behavioral Pharma (United States) · USCzech Academy of Sciences, Institute of Physiology · CZJohannes Gutenberg University Mainz · DEUniversity Hospital Münster · DEAugenstern · DEEvangelisches Krankenhaus Bielefeld · DEExpedeon (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Granulocyte-colony stimulating factor (G-CSF) is a hematopoietic growth factor that controls proliferation and differentiation of neural stem cells. Although recent studies have begun to explore G-CSF-related mechanisms of action in various disease models, little is known about its function in the healthy brain. In the present study, the effect of G-CSF deficiency on memory formation and motor skills was investigated. The impact of G-CSF deficiency on the structural integrity of the hippocampus was evaluated by analyzing the generation of doublecortin-expressing cells, the amount of bromodeoxyurine-labeled cells, the dendritic complexity in hippocampal neurons, the binding densities of NMDA and GABA(A) receptors and the induction of long-term potentiation (LTP). G-CSF deficiency caused a disruption in memory formation and in the development of motor skills. These impairments were associated with reduced ligand binding densities of NMDA receptors in hippocampal subfields CA3 and the dentate gyrus. The reduced excitation was potentiated by increased ligand binding densities of GABA(A) receptors resulting in a relative shift in favor of inhibition and impaired behavioral performance. These alterations were accompanied by impaired induction of LTP in the CA1 region. Moreover, G-CSF deficiency led to decreased dendritic complexity in hippocampal neurons in the dentate gyrus and the CA1 region. G-CSF deficiency also caused a reduction of neuronal precursor cells in the dentate gyrus. These findings confirm G-CSF as an essential neurotrophic factor, and point to a role in the proliferation, differentiation and functional integration of neural cells necessary for the structural and functional integrity of the hippocampal formation.

Indexed as

Analysis of VarianceAnimalsAutoradiographyBehavior, AnimalBiophysicsBromodeoxyuridineCell CountDizocilpine MaleateDoublecortin Domain ProteinsElectric StimulationExploratory BehaviorGene Expression RegulationGranulocyte Colony-Stimulating FactorHippocampusLong-Term PotentiationMaleBromodeoxyuridineDizocilpine MaleateDoublecortin Domain ProteinsGranulocyte Colony-Stimulating FactorMicrotubule-Associated ProteinsMuscimolNeuropeptidesPhosphopyruvate HydrataseReceptors, GABAReceptors, N-Methyl-D-AspartateTritium

Identifiers

PMID19759304
PMCPMC6665757
OpenAlexW2056757429

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.