ReviewClinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology2023
The Role of Glutamate Underlying Treatment-resistant Depression.
Review in Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Treatment with perampanel alleviates depression-like behavior in mice via modulating GluN2B expression to improve excitatory synaptic transmission.Translational psychiatry · 2026Article
- Recent developments in imaging transcriptomics for psychiatric disorders.Psychoradiology · 2026Review
- Designing Neural Dynamics: From Digital Twin Modeling to Regeneration.International journal of molecular sciences · 2025Review
- Molecular Characteristics of Spontaneous Remission in Major Depressive Disorder: Changes in Serum Acetylcarnitine and Glycerophosphcholine Levels.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Article
- Modulation of neuroimmune cytokine networks by antidepressants: implications in mood regulation.Translational psychiatry · 2025Review
- Symptom networks in major depressive disorder and treatment response: special focus on TRD.European psychiatry : the journal of the Association of European Psychiatrists · 2025Article
- Patient Experience with Intranasal Esketamine in Treatment-Resistant Depression: Insights from a Multicentric Italian Study (REAL-ESKperience).Journal of personalized medicine · 2025Article
- From Stress to Synapse: The Neuronal Atrophy Pathway to Mood Dysregulation.International journal of molecular sciences · 2025Review
- Esketamine reduces postoperative depression in breast cancer through TREK-1 channel inhibition and neurotransmitter modulation.Cancer cell international · 2025Article
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Is there a risk of esketamine misuse in clinical practice?Therapeutic advances in drug safety · 2025Review
- GluN2A: A Promising Target for Developing Novel Antidepressants.The international journal of neuropsychopharmacology · 2024Review
- Heart Rate Variability as a Potential Predictor of Response to Intranasal Esketamine in Patients with Treatment-Resistant Depression: A Preliminary Report.Journal of clinical medicine · 2024Article
- Glutamate concentrations related to depression and mania symptoms in patients with Graves' disease: A 1H-magnetic resonance spectroscopy study.The Kaohsiung journal of medical sciences · 2024Article
- Article
- Very Low-Dose Sublingual Ketamine for Borderline Personality Disorder and Treatment-Resistant Depression.Cureus · 2024Article
- Synaptotagmin-4 induces anhedonic responses to chronic stress via BDNF signaling in the medial prefrontal cortex.Experimental & molecular medicine · 2024Article
- Pharmacovigilance of esketamine nasal spray: an analysis of the FDA adverse event reporting system database.Frontiers in pharmacology · 2024Article
- The Patient's Perspective on the Effects of Intranasal Esketamine in Treatment-Resistant Depression.Brain sciences · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monoamine hypothesis has significantly improved our understanding of mood disorders and their treatment by linking monoaminergic abnormalities to the pathophysiology of mood disorders. Even 50 years after the monoamine hypothesis was established, some patients do not respond to treatments for depression, including selective serotonin reuptake drugs. Accumulating evidence shows that patients with treatment-resistant depression (TRD) have severe abnormalities in the neuroplasticity and neurotrophic factor pathways, indicating that different treatment approaches may be necessary. Therefore, the glutamate hypothesis is gaining attention as a novel hypothesis that can overcome monoamine restrictions. Glutamate has been linked to structural and maladaptive morphological alterations in several brain areas associated with mood disorders. Recently, ketamine, an N-methyl-D-aspartate receptor (NMDAR) antagonist, has shown efficacy in TRD treatment and has received the U.S. Food and Drug Administration approval, revitalizing psychiatry research. However, the mechanism by which ketamine improves TRD remains unclear. In this review, we re-examined the glutamate hypothesis, bringing the glutamate system onboard to join the modulation of the monoamine systems, emphasizing the most prominent ketamine antidepressant mechanisms, such as NMDAR inhibition and NMDAR disinhibition in GABAergic interneurons. Furthermore, we discuss the animal models used in preclinical studies and the sex differences in the effects of ketamine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.