G protein-biased LPAR1 agonism of prototypic antidepressants: Implication in the identification of novel therapeutic target for depression.


Journal

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
ISSN: 1740-634X
Titre abrégé: Neuropsychopharmacology
Pays: England
ID NLM: 8904907

Informations de publication

Date de publication:
06 Sep 2023
Historique:
received: 09 03 2023
accepted: 24 08 2023
revised: 01 08 2023
pubmed: 7 9 2023
medline: 7 9 2023
entrez: 6 9 2023
Statut: aheadofprint

Résumé

Prototypic antidepressants, such as tricyclic/tetracyclic antidepressants (TCAs), have multiple pharmacological properties and have been considered to be more effective than newer antidepressants, such as selective serotonin reuptake inhibitors, in treating severe depression. However, the clinical contribution of non-monoaminergic effects of TCAs remains elusive. In this study, we discovered that amitriptyline, a typical TCA, directly binds to the lysophosphatidic acid receptor 1 (LPAR1), a G protein-coupled receptor, and activates downstream G protein signaling, while exerting a little effect on β-arrestin recruitment. This suggests that amitriptyline acts as a G protein-biased agonist of LPAR1. This biased agonism was specific to TCAs and was not observed with other antidepressants. LPAR1 was found to be involved in the behavioral effects of amitriptyline. Notably, long-term infusion of mouse hippocampus with the potent G protein-biased LPAR agonist OMPT, but not the non-biased agonist LPA, induced antidepressant-like behavior, indicating that G protein-biased agonism might be necessary for the antidepressant-like effects. Furthermore, RNA-seq analysis revealed that LPA and OMPT have opposite patterns of gene expression changes in the hippocampus. Pathway analysis indicated that long-term treatment with OMPT activated LPAR1 downstream signaling (Rho and MAPK), whereas LPA suppressed LPAR1 signaling. Our findings provide insights into the mechanisms underlying the non-monoaminergic antidepressant effects of TCAs and identify the G protein-biased agonism of LPAR1 as a promising target for the development of novel antidepressants.

Identifiants

pubmed: 37673966
doi: 10.1038/s41386-023-01727-9
pii: 10.1038/s41386-023-01727-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : MEXT | Japan Society for the Promotion of Science (JSPS)
ID : 18H02756
Organisme : MEXT | Japan Society for the Promotion of Science (JSPS)
ID : 21K07501
Organisme : MEXT | Japan Society for the Promotion of Science (JSPS)
ID : 21H04791 and 21H051130
Organisme : MEXT | Japan Science and Technology Agency (JST)
ID : PMJFR215T and JPMJMS2023
Organisme : Japan Agency for Medical Research and Development (AMED)
ID : 21gm0010004h9905

Informations de copyright

© 2023. The Author(s).

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Auteurs

Naoto Kajitani (N)

Department of Neuropsychiatry, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.
Center for Metabolic Regulation of Healthy Aging, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.
Division of Psychiatry and Neuroscience, Institute for Clinical Research, National Hospital Organization Kure Medical Center and Chugoku Cancer Center, Kure, 737-0023, Japan.

Mami Okada-Tsuchioka (M)

Division of Psychiatry and Neuroscience, Institute for Clinical Research, National Hospital Organization Kure Medical Center and Chugoku Cancer Center, Kure, 737-0023, Japan.

Asuka Inoue (A)

Laboratory of Molecular and Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan.

Kanako Miyano (K)

Department of Pain Control Research, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Division of Cancer Pathophysiology, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.

Takeshi Masuda (T)

Department of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, 862-0973, Japan.

Shuken Boku (S)

Department of Neuropsychiatry, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.

Kazuya Iwamoto (K)

Department of Molecular Brain Science, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.

Sumio Ohtsuki (S)

Department of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, 862-0973, Japan.

Yasuhito Uezono (Y)

Department of Pain Control Research, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.

Junken Aoki (J)

Department of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan.

Minoru Takebayashi (M)

Department of Neuropsychiatry, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan. mtakebayashi@kumamoto-u.ac.jp.
Division of Psychiatry and Neuroscience, Institute for Clinical Research, National Hospital Organization Kure Medical Center and Chugoku Cancer Center, Kure, 737-0023, Japan. mtakebayashi@kumamoto-u.ac.jp.

Classifications MeSH