Skip to content

Role of mTOR1 signaling in the antidepressant effects of ketamine and the potential of mTORC1 activators as novel antidepressants.

Taro Kato

Neuropharmacology February 1, 2023 DOI: 10.1016/j.neuropharm.2022.109325 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Intervention Ketamine
Topics Depression Ketamine Esketamine
Keywords Antidepressants Glutamatergic signaling Mtorc1
Key findings The authors argue that mTORC1 signaling and the resulting increase in synapse formation in the medial prefrontal cortex play a key role in ketamine's rapid antidepressant effects, and propose that mTORC1 signaling itself could be a drug discovery target.

Abstract

Conventional antidepressant medications act on monoaminergic systems and have important limitations, including a therapeutic delay of weeks to months and low rates of efficacy. Recently, clinical findings have indicated that ketamine, a dissociative anesthetic that blocks N-methyl-d-aspartate receptor channel activity, causes rapid and long-lasting antidepressant effects. Although the exact mechanisms underlying the antidepressant effects of ketamine are not fully known, preclinical studies have demonstrated a key role for mechanistic target of rapamycin complex 1 (mTORC1) signaling and a subsequent increase in synapse formation in the medial prefrontal cortex. In this review, we discuss the role of mTORC1 and its subsequent signaling cascade in the antidepressant effects of ketamine and other compounds with glutamatergic mechanisms of action. We also present the possibility that mTORC1 signaling itself is a drug discovery target.

Comparable studies

Other narrative reviews on ketamine for depression, most cited first.

Explore topics

By condition and practice