Evidence map›Paper›PMID 39775023›Full record

ArticlePsychopharmacology2025

Investigating the role of GPR39 in treatment of stress-induced depression and anxiety.

Dominika Siodłak, Urszula Doboszewska, Gabriel Nowak, Piotr Wlaź, Katarzyna Mlyniec

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Article in Psychopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Dominika SiodłakDepartment of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688, Kraków, Poland.
Urszula DoboszewskaDepartment of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688, Kraków, Poland.
Gabriel NowakDepartment of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688, Kraków, Poland.
Piotr WlaźDepartment of Animal Physiology and Pharmacology, Institute of Biological Sciences, Faculty of Biology and Biotechnology, Maria Curie-Sklodowska University, Akademicka 19, 20-033, Lublin, Poland.
Katarzyna MlyniecDepartment of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688, Kraków, Poland. katarzyna.mlyniec@uj.edu.pl.ORCID http://orcid.org/0000-0002-9257-8154

Funding

Narodowe Centrum Nauki UMO-2018/31/B/NZ7/00247
6 · The paper itself

Abstract

rationaleChronic stress is one of the leading causes of depression. Yet, knowledge of the pathomechanism of this process still eludes us. Chronic unpredictable mild stress (CUMS) model of depression enables researchers to look for a root cause of the disease in mice by mimicking a stressful human environment.

objectiveSince zinc has already been shown to impact the treatment of depression, in our study we aimed to shed light on the role of the zinc receptor GPR39 in stress-induced depression. We also aimed to highlight the role of GPR39 activation in monoamine-based antidepressant treatment.

methodsUsing large battery of behavioural tests, we provided a detailed description of CUMS-induced phenotype in both - CD-1 and GPR39 knock-out mice.

resultsOur experiments showed that combined treatment with TC-G 1008 (GPR39 agonist) and antidepressants produces stronger antidepressant-like effect of classic antidepressants. We also demonstrated the inter-strain differences in stress response and the greater stress susceptibility of GPR39 knock-out mice. The lack of GPR39 expression also either diminished or completely abolished the response to treatment with different antidepressants combined with TC-G 1008.

conclusionsThe results show that GPR39 KO mice are more susceptible to chronic stress and that they are non-responsive to SSRI treatment. Utilizing various behavioural tests gave us much broader understanding not only of the role of GPR39 in depression treatment, but also of the importance of detailed behavioural description in a proper interpretation of the results. Further research with known selective agonists and antagonists of GPR39 will be necessary to understand the full potential of this receptor as a pharmacological target.

Indexed as

Antidepressive AgentsAnxietyDepressionReceptors, G-Protein-CoupledStress, PsychologicalAnimalsBehavior, AnimalDisease Models, AnimalMaleMiceMice, KnockoutAntidepressive AgentsGPR39 protein, mouseReceptors, G-Protein-CoupledCUMSDepressionGPR39Monoamine-based antidepressantZinc

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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.