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The N-methyl-d-aspartate receptor hypothesis of ketamine's antidepressant action: evidence and controversies.

Yihao Jiang, Yiyan Dong, Hailan Hu

Philosophical transactions of the Royal Society of London. Series B, Biological sciences July 29, 2024 DOI: 10.1098/rstb.2023.0225 (opens in new tab)

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AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Depression Ketamine Esketamine
Keywords Nmdar hypothesis Nmdar inhibitors Antidepressant efficacy Depression treatment Ketamine therapy Nmdar research Antidepressant mechanisms Rapid-acting antidepressants
Key findings Ketamine's antidepressant mechanisms involve both NMDAR-dependent and independent actions, with ongoing debate from clinical results of other NMDAR inhibitors.

Abstract

Substantial clinical evidence has unravelled the superior antidepressant efficacy of ketamine: in comparison to traditional antidepressants targeting the monoamine systems, ketamine, as an N-methyl-d-aspartate receptor (NMDAR) antagonist, acts much faster and more potently. Surrounding the antidepressant mechanisms of ketamine, there is ample evidence supporting an NMDAR-antagonism-based hypothesis. However, alternative arguments also exist, mostly derived from the controversial clinical results of other NMDAR inhibitors. In this article, we first summarize the historical development of the NMDAR-centred hypothesis of rapid antidepressants. We then classify different NMDAR inhibitors based on their mechanisms of inhibition and evaluate preclinical as well as clinical evidence of their antidepressant effects. Finally, we critically analyse controversies and arguments surrounding ketamine's NMDAR-dependent and NMDAR-independent antidepressant action. A better understanding of ketamine's molecular targets and antidepressant mechanisms should shed light on the future development of better treatment for depression. This article is part of a discussion meeting issue 'Long-term potentiation: 50 years on'.

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