GPR56/ADGRG1 is associated with response to antidepressant treatment

Raoul Belzeaux, Victor Gorgievski, Laura M. Fiori, Juan Pablo Lopez, Julien Grenier, Rixing Lin, Corina Nagy, El Chérif Ibrahim, Eduardo Gascon, Philippe Courtet, Stéphane Richard-Devantoy, Marcelo Berlim, Eduardo Chachamovich, Jean-François Théroux, Sylvie Dumas, Bruno Giros, Susan Rotzinger, Claudio N. Soares, Jane A. Foster, Naguib Mechawar, Gregory G. Tall, Eleni T. Tzavara, Sidney H. Kennedy and Gustavo Turecki ()
Additional contact information
Raoul Belzeaux: McGill University
Victor Gorgievski: CNRS (Integrative Neuroscience and Cognition Center, UMR 8002)
Laura M. Fiori: McGill University
Juan Pablo Lopez: McGill University
Julien Grenier: Université Paris Descartes
Rixing Lin: McGill University
Corina Nagy: McGill University
El Chérif Ibrahim: Hôpital Sainte Marguerite, Pôle de psychiatrie
Eduardo Gascon: Hôpital Sainte Marguerite, Pôle de psychiatrie
Philippe Courtet: Fondation FondaMental
Stéphane Richard-Devantoy: McGill University
Marcelo Berlim: McGill University
Eduardo Chachamovich: McGill University
Jean-François Théroux: McGill University
Sylvie Dumas: Oramacell
Bruno Giros: McGill University
Susan Rotzinger: University Health Network, Krembil Research Institute, University of Toronto
Claudio N. Soares: Centre for Depression and Suicide Studies
Jane A. Foster: University Health Network, Krembil Research Institute, University of Toronto
Naguib Mechawar: McGill University
Gregory G. Tall: University of Michigan
Eleni T. Tzavara: Fondation FondaMental
Sidney H. Kennedy: University Health Network, Krembil Research Institute, University of Toronto
Gustavo Turecki: McGill University

Nature Communications, 2020, vol. 11, issue 1, 1-10

Abstract: Abstract It remains unclear why many patients with depression do not respond to antidepressant treatment. In three cohorts of individuals with depression and treated with serotonin-norepinephrine reuptake inhibitor (N = 424) we show that responders, but not non-responders, display an increase of GPR56 mRNA in the blood. In a small group of subjects we also show that GPR56 is downregulated in the PFC of individuals with depression that died by suicide. In mice, we show that chronic stress-induced Gpr56 downregulation in the blood and prefrontal cortex (PFC), which is accompanied by depression-like behavior, and can be reversed by antidepressant treatment. Gpr56 knockdown in mouse PFC is associated with depressive-like behaviors, executive dysfunction and poor response to antidepressant treatment. GPR56 peptide agonists have antidepressant-like effects and upregulated AKT/GSK3/EIF4 pathways. Our findings uncover a potential role of GPR56 in antidepressant response.

Date: 2020
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DOI: 10.1038/s41467-020-15423-5

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