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Role of the mTOR signaling pathway in the rapid antidepressant action of ketamine.

Kenji Hashimoto

Expert Review of Neurotherapeutics January 2011 DOI: 10.1586/ern.10.176 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Commentary Randomized Placebo-controlled Double-blind Peer reviewed
Intervention Ketamine
Dose 0.5 mg/kg
Topics Esketamine Ketamine
Key points The commentary discusses how a single subanesthetic dose of ketamine (0.5 mg/kg) produces rapid antidepressant effects in treatment-resistant major depressive disorder, and contextualizes Li et al.'s findings that the mTOR signaling pathway, involved in protein synthesis and synaptic plasticity, may underlie these effects.

Abstract

Some patients with major depressive disorder remain resistant to antidepressant medication. A randomized, placebo-controlled, double-blind trial demonstrated that a single subanesthetic dose (0.5 mg/kg) of the N-methyl-D-aspartate receptor antagonist ketamine caused a rapid antidepressant effect within hours in treatment-resistant patients with major depressive disorder. However, the precise cellular mechanisms underlying ketamine's rapid antidepressant actions were unclear, although it is proposed that the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor might be involved in these mechanisms. Recently, Li et al. reported the role of the mammalian target of rapamycin (mTOR) signaling pathway, a ubiquitous protein kinase involved in protein synthesis and synaptic plasticity, in ketamine's rapid antidepressant effects. Here, these findings are put into context and their significance is discussed.

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