ReviewDialogues in clinical neuroscience2014
Pathophysiology of depression and innovative treatments: remodeling glutamatergic synaptic connections.
Review in Dialogues in clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
120 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.
- Diminished reward responsiveness is associated with lower reward network GluCEST: an ultra-high field glutamate imaging study.Molecular psychiatry · 2021Pooled it
- Safety and Efficacy of the NMDA-2b-Selective Negative Allosteric Modulator BI 1569912: A Phase Ib Randomized Trial in Major Depressive Disorder.Clinical pharmacology and therapeutics · 2025Trial
- Default mode network connectivity change corresponds to ketamine's delayed glutamatergic effects.European archives of psychiatry and clinical neuroscience · 2020Trial
- Shank3 as a potential biomarker of antidepressant response to ketamine and its neural correlates in bipolar depression.Journal of affective disorders · 2015Trial
- NMDA subunit 2B-selective negative allosteric modulator satoprodil (BI 1569912) as mono- and adjunctive therapy in patients with major depressive disorder: results from two phase 2 randomized, controlled trials.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Metal Ions in Longgu (Fossilized Bone) as a Natural Synergistic Network for Multi-Target Therapy in Psychiatric Disorders.Chemistry & biodiversity · 2026Review
- BDNF and GSK-3β signaling in depression: molecular mechanisms underlying neural plasticity dysfunction.Molecular biology reports · 2026Review
- Intermittent Ketamine and Neuromodulation Treatment Evoke Synergistic Antidepressant-Relevant Action.Biological psychiatry · 2026Article
- Synaptic Plasticity-Intrinsic Excitability and Antidepressant Discovery.Biomedicines · 2026Review
- A Time-Sensitive Plasticity Distinguishes the Rapid and Sustained Synaptic Actions of Ketamine from Its (2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Review
- Multimodal Pharmacological Assessment ofFood science & nutrition · 2025Article
- Cannabidiol reverses depression-like behaviors by enhancing hippocampal synaptic plasticity in rats with chronic restraint stress.Veterinary world · 2025Article
- Mechanisms of angiotensin II to induce depression in diabetes.Diabetology international · 2025Review
- Bioactive ketamine metabolite exerts in vivo neuroplastogenic effects to improve hippocampal function in a treatment-resistant depression model.Cell reports · 2025Article
- Delta opioid receptor agonists activate PI3K-mTORC1 signaling in parvalbumin-positive interneurons in mouse infralimbic prefrontal cortex to exert acute antidepressant-lie effects.Molecular psychiatry · 2025Article
- Rapid hippocampal synaptic potentiation induced by ketamine metabolite (2R,6R)-hydroxynorketamine persistently primes synaptic plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Effects of tianeptine on mTORC1-mediated neuronal autophagy in primary rat hippocampal neurons under nutrient deprivation.Scientific reports · 2025Article
- Demystifying the Antidepressant Mechanism of Action of Stinels, a Novel Class of Neuroplastogens: Positive Allosteric Modulators of the NMDA Receptor.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Despite the complexity and heterogeneity of mood disorders, basic and clinical research studies have begun to elucidate the pathophysiology of depression and to identify rapid, efficacious antidepressant agents. Stress and depression are associated with neuronal atrophy, characterized by loss of synaptic connections in key cortical and limbic brain regions implicated in depression. This is thought to occur in part via decreased expression and function of growth factors, such as brain-derived neurotrophic factor (BDNF), in the prefrontal cortex (PFC) and hippocampus. These structural alterations are difficult to reverse with typical antidepressants. However, recent studies demonstrate that ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that produces rapid antidepressant actions in treatment-resistant depressed patients, rapidly increases spine synapses in the PFC and reverses the deficits caused by chronic stress. This is thought to occur by disinhibition of glutamate transmission, resulting in a rapid but transient burst of glutamate, followed by an increase in BDNF release and activation of downstream signaling pathways that stimulate synapse formation. Recent work demonstrates that the rapid-acting antidepressant effects of scopolamine, a muscarinic receptor antagonist, are also associated with increased glutamate transmission and synapse formation. These findings have resulted in testing and identification of additional targets and agents that influence glutamate transmission and have rapid antidepressant actions in rodent models and in clinical trials. Together these studies have created tremendous excitement and hope for a new generation of rapid, efficacious antidepressants.
Indexed as
Identifiers
24733968PMC3984887W184284683What OpenQuestion holds
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.