N-Methyl-D-aspartate receptor antagonist d-methadone produces rapid, mTORC1-dependent antidepressant effects.


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:
12 2019
Historique:
received: 21 06 2019
accepted: 20 08 2019
revised: 16 08 2019
pubmed: 28 8 2019
medline: 9 7 2020
entrez: 28 8 2019
Statut: ppublish

Résumé

Currently available antidepressants have a delayed onset and limited efficacy, highlighting the need for new, rapid and more efficacious agents. Ketamine, an NMDA receptor antagonist, has emerged as a new rapid-acting antidepressant, effective even in treatment resistant patients. However, ketamine induces undesired psychotomimetic and dissociative side effects that limit its clinical use. The d-stereoisomer of methadone (dextromethadone; REL-1017) is a noncompetitive NMDA receptor antagonist with an apparently favorable safety and tolerability profile. The current study examined the rapid and sustained antidepressant actions of d-methadone in several behavioral paradigms, as well as on mTORC1 signaling and synaptic changes in the medial prefrontal cortex (mPFC). A single dose of d-methadone promoted rapid and sustained antidepressant responses in the novelty-suppressed feeding test (NSFT), a measure of anxiety, and in the female urine sniffing test (FUST), a measure of motivation and reward. D-methadone also produced a rapid reversal of the sucrose preference deficit, a measure of anhedonia, in rats exposed to chronic unpredictable stress. D-methadone increased phospho-p70S6 kinase, a downstream target of mTORC1 in the mPFC, and intra-mPFC infusion of the selective mTORC1 inhibitor rapamycin blocked the antidepressant actions of d-methadone in the FUST and NSFT. D-methadone administration also increased levels of the synaptic proteins, PSD95, GluA1, and Synapsin 1 and enhanced synaptic function in the mPFC. Studies in primary cortical cultures show that d-methadone also increases BDNF release, as well as phospho-p70S6 kinase. These findings indicate that d-methadone induces rapid antidepressant actions through mTORC1-mediated synaptic plasticity in the mPFC similar to ketamine.

Identifiants

pubmed: 31454827
doi: 10.1038/s41386-019-0501-x
pii: 10.1038/s41386-019-0501-x
pmc: PMC6898593
doi:

Substances chimiques

Antidepressive Agents 0
D-methadone 0
Receptors, N-Methyl-D-Aspartate 0
Ketamine 690G0D6V8H
Mechanistic Target of Rapamycin Complex 1 EC 2.7.11.1
Methadone UC6VBE7V1Z

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2230-2238

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Auteurs

Manoela V Fogaça (MV)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA.

Kenichi Fukumoto (K)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA.

Tina Franklin (T)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA.

Rong-Jian Liu (RJ)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA.

Catharine H Duman (CH)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA.

Ottavio V Vitolo (OV)

Relmada Therapeutics Inc., 880 Third Ave, 12th floor, New York, NY, 10022, USA.

Ronald S Duman (RS)

Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT, 06520, USA. ronald.duman@yale.edu.

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