Evidence map›Paper›PMID 35618883›Full record

ArticleMolecular psychiatry2022

Elevated endogenous GDNF induces altered dopamine signalling in mice and correlates with clinical severity in schizophrenia.

Kärt Mätlik, Daniel R Garton, Ana R Montaño-Rodríguez, Soophie Olfat, Feride Eren, Laoise Casserly, Anastasios Damdimopoulos, Anne Panhelainen, L Lauriina Porokuokka, Jaakko J Kopra and 13 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 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

23 authors at 6 institutions in 2 countries.

Kärt MätlikDepartment of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland. kmatlik01@rockefeller.edu.ORCID http://orcid.org/0000-0003-1777-5614
Daniel R Garton *Department of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Ana R Montaño-Rodríguez *Department of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Soophie Olfat *Department of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Feride ErenDepartment of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-6068-5329
Laoise CasserlyDepartment of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Anastasios DamdimopoulosDepartment of Biosciences and Nutrition, Karolinska Institutet, 14183, Huddinge, Sweden.
Anne PanhelainenInstitute of Biotechnology, University of Helsinki, 00014, Helsinki, Finland.
L Lauriina PorokuokkaDepartment of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Jaakko J KopraDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, University of Helsinki, 00014, Helsinki, Finland.
Giorgio TurconiDepartment of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland.
Nadine SchweizerDivision of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, 14183, Huddinge, Sweden.
Erika BereczkiDivision of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, 14183, Huddinge, Sweden.
Fredrik PiehlDepartment of Clinical Neuroscience, Neuroimmunology Unit, Karolinska Institutet, Karolinska University Hospital, 17177, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-8329-5219
Göran EngbergDepartment of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-1659-5232
Simon CervenkaCentre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Services, Region Stockholm, 17177, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-8103-6977
T Petteri PiepponenDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, University of Helsinki, 00014, Helsinki, Finland.ORCID http://orcid.org/0000-0002-2318-1612
Fu-Ping ZhangResearch Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine and Turku Center for Disease Modeling, University of Turku, 20520, Turku, Finland.
Petra SipiläResearch Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine and Turku Center for Disease Modeling, University of Turku, 20520, Turku, Finland.
Johan JakobssonLaboratory of Molecular Neurogenetics, Department of Experimental Medical Science, Wallenberg Neuroscience Center and Lund Stem Cell Center, BMC A11, Lund University, 221 84, Lund, Sweden.ORCID http://orcid.org/0000-0003-0669-7673
Carl M SellgrenDepartment of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden.
Sophie ErhardtDepartment of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-7359-5250
Jaan-Olle AndressooDepartment of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science, University of Helsinki, 00290, Helsinki, Finland. jaan-olle.andressoo@helsinki.fi.ORCID http://orcid.org/0000-0002-0271-3157
University of Helsinki · FIKarolinska Institutet · SEKarolinska University Hospital · SELund University · SEUniversity of Turku · FIUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Presynaptic increase in striatal dopamine is the primary dopaminergic abnormality in schizophrenia, but the underlying mechanisms are not understood. Here, we hypothesized that increased expression of endogenous GDNF could induce dopaminergic abnormalities that resemble those seen in schizophrenia. To test the impact of GDNF elevation, without inducing adverse effects caused by ectopic overexpression, we developed a novel in vivo approach to conditionally increase endogenous GDNF expression. We found that a 2-3-fold increase in endogenous GDNF in the brain was sufficient to induce molecular, cellular, and functional changes in dopamine signalling in the striatum and prefrontal cortex, including increased striatal presynaptic dopamine levels and reduction of dopamine in prefrontal cortex. Mechanistically, we identified adenosine A2a receptor (A

Indexed as

DopamineSchizophreniaAnimalsCorpus StriatumGlial Cell Line-Derived Neurotrophic FactorMiceSignal TransductionDopamineGlial Cell Line-Derived Neurotrophic Factor

Identifiers

PMID35618883
PMCPMC9708553
OpenAlexW4281552392

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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.