Esmethadone (REL-1017) and Other Uncompetitive NMDAR Channel Blockers May Improve Mood Disorders via Modulation of Synaptic Kinase-Mediated Signaling.
N-methyl-D-aspartate receptor
REL-1017
d-methadone
depression
dextromethorphan
esketamine
esmethadone
ketamine
major depressive disorder
neural plasticity
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
13 Oct 2022
13 Oct 2022
Historique:
received:
31
08
2022
revised:
04
10
2022
accepted:
10
10
2022
entrez:
27
10
2022
pubmed:
28
10
2022
medline:
29
10
2022
Statut:
epublish
Résumé
This article presents a mechanism of action hypothesis to explain the rapid antidepressant effects of esmethadone (REL-1017) and other uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonists and presents a corresponding mechanism of disease hypothesis for major depressive disorder (MDD). Esmethadone and other uncompetitive NMDAR antagonists may restore physiological neural plasticity in animal models of depressive-like behavior and in patients with MDD via preferential tonic block of pathologically hyperactive GluN2D subtypes. Tonic Ca
Identifiants
pubmed: 36293063
pii: ijms232012196
doi: 10.3390/ijms232012196
pmc: PMC9602945
pii:
doi:
Substances chimiques
Receptors, N-Methyl-D-Aspartate
0
Antidepressive Agents
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Relmada Therapeutics
ID : VDD9974
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