Evidence map›Paper›PMID 33686166›Full record

ArticleScientific reports2021

Slc1a3-2A-CreERT2 mice reveal unique features of Bergmann glia and augment a growing collection of Cre drivers and effectors in the 129S4 genetic background.

Lech Kaczmarczyk, Nicole Reichenbach, Nelli Blank, Maria Jonson, Lars Dittrich, Gabor C Petzold, Walker S Jackson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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  6. A NaFrontiers in molecular neuroscience · 2025
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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

7 authors at 2 institutions in 2 countries.

Lech KaczmarczykDepartment of Biomedical and Clinical Sciences, Wallenberg Center for Molecular Medicine, Linköping University, Linköping, Sweden.
Nicole ReichenbachGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Nelli BlankGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Maria JonsonDepartment of Biomedical and Clinical Sciences, Wallenberg Center for Molecular Medicine, Linköping University, Linköping, Sweden.
Lars DittrichGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Gabor C PetzoldGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Walker S JacksonDepartment of Biomedical and Clinical Sciences, Wallenberg Center for Molecular Medicine, Linköping University, Linköping, Sweden. walker.jackson@liu.se.
German Center for Neurodegenerative Diseases · DELinköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic variation is a primary determinant of phenotypic diversity. In laboratory mice, genetic variation can be a serious experimental confounder, and thus minimized through inbreeding. However, generalizations of results obtained with inbred strains must be made with caution, especially when working with complex phenotypes and disease models. Here we compared behavioral characteristics of C57Bl/6-the strain most widely used in biomedical research-with those of 129S4. In contrast to 129S4, C57Bl/6 demonstrated high within-strain and intra-litter behavioral hyperactivity. Although high consistency would be advantageous, the majority of disease models and transgenic tools are in C57Bl/6. We recently established six Cre driver lines and two Cre effector lines in 129S4. To augment this collection, we genetically engineered a Cre line to study astrocytes in 129S4. It was validated with two Cre effector lines: calcium indicator gCaMP5g-tdTomato and RiboTag-a tool widely used to study cell type-specific translatomes. These reporters are in different genomic loci, and in both the Cre was functional and astrocyte-specific. We found that calcium signals lasted longer and had a higher amplitude in cortical compared to hippocampal astrocytes, genes linked to a single neurodegenerative disease have highly divergent expression patterns, and that ribosome proteins are non-uniformly expressed across brain regions and cell types.

Indexed as

Excitatory Amino Acid Transporter 1Neurodegenerative DiseasesAnimalsIntegrasesMiceMice, TransgenicNeurogliaCre recombinaseExcitatory Amino Acid Transporter 1IntegrasesSlc1a3 protein, mouse

Identifiers

PMID33686166
PMCPMC7940647
OpenAlexW3134521269

What OpenQuestion holds

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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.