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The review discusses the role of glutamate in treatment-resistant depression (TRD) and highlights the limitations of the monoamine hypothesis in explaining treatment outcomes. It emphasizes the potential of ketamine, an NMDAR antagonist, as a rapid-acting treatment for TRD and explores its mechanisms of action, including effects on neuroplasticity and neurotrophic factors. The review also addresses the need for alternative treatment approaches for TRD patients who do not respond to traditional antidepressan

Author

Gakungu Shabanl

Language

EN