Trial reportBiological psychiatry2012
Synaptic potentiation is critical for rapid antidepressant response to ketamine in treatment-resistant major depression.
Trial report in Biological psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 198 citations in OpenAlex.
- A Meta-Analysis of Magnetic Resonance Spectroscopy Studies on Glutamatergic Neurometabolite Levels in Major Depressive Disorder.Depression and anxiety · 2025Pooled it
- Brain-based correlates of antidepressant response to ketamine: a comprehensive systematic review of neuroimaging studies.The lancet. Psychiatry · 2023Pooled it
- High-order brain interactions during ketamine-induced state changes: A functional marker of response in late-life treatment-resistant depression?Translational psychiatry · 2026Trial
- Effect of Anterior Quadratus Lumborum Block at the Lateral Supra-Arcuate Ligament Combined with Esketamine on the Quality of Postoperative Recovery After Laparoscopic Radical Surgery for Elderly Patients with Colorectal Cancer: A Randomized Controlled Trial.Drug design, development and therapy · 2026Trial
- A randomized, placebo-controlled, cross-over trial of ketamine in Rett syndrome.Journal of neurodevelopmental disorders · 2025Trial
- Neural complexity EEG biomarkers of rapid and post-rapid ketamine effects in late-life treatment-resistant depression: a randomized control trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Trial
- Magnetoencephalography biomarkers of suicide attempt history and antidepressant response to ketamine in treatment-resistant major depression.Journal of affective disorders · 2022Trial
- Ketamine Alters Electrophysiological Responses to Emotional Faces in Major Depressive Disorder.Journal of affective disorders · 2021Trial
- Ketamine metabolites, clinical response, and gamma power in a randomized, placebo-controlled, crossover trial for treatment-resistant major depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Trial
- Magnetoencephalographic Correlates of Suicidal Ideation in Major Depression.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2020Trial
- A randomized, placebo-controlled pilot trial of the delta opioid receptor agonist AZD2327 in anxious depression.Psychopharmacology · 2016Trial
- Improvement in suicidal ideation after ketamine infusion: relationship to reductions in depression and anxiety.Journal of psychiatric research · 2014Trial
- Clinical predictors of ketamine response in treatment-resistant major depression.The Journal of clinical psychiatry · 2014Trial
- Plasma brain derived neurotrophic factor (BDNF) and response to ketamine in treatment-resistant depression.The international journal of neuropsychopharmacology · 2014Trial
- Enhancing plasticity to treat depression and other central nervous system diseases using event-driven pharmacology.Journal of psychopharmacology (Oxford, England) · 2026Review
- TrkB/mGluR5 cross-talk underlies a synaptic metaplasticity mechanism of ketamine.Science advances · 2026Article
- Antidepressant-like effects of extinction learning as an animal model of behavioral therapy.Molecular psychiatry · 2026Article
- The Monoamine-Glutamate Continuum of Depression: A Neurobiological Framework for Precision Psychiatry.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Role of neural oscillations in depression: highlights on gamma oscillations.Translational psychiatry · 2026Review
- Sympathetic activation but not dissociation linked to ketamine's sustained antidepressant effect.Therapeutic advances in psychopharmacology · 2026Article
38 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundClinical evidence that ketamine, a nonselective N-methyl-D-aspartate receptor (NMDAR) antagonist, has therapeutic effects within hours in people suffering from depression suggests that modulating glutamatergic neurotransmission is a fundamental step in alleviating the debilitating symptoms of mood disorders. Acutely, ketamine increases extracellular glutamate levels, neuronal excitability, and spontaneous γ oscillations, but it is unknown whether these effects are key to the mechanism of antidepressant action of ketamine.
methodsTwenty drug-free major depressive disorder patients received a single, open-label intravenous infusion of ketamine hydrochloride (.5 mg/kg). Magnetoencephalographic recordings were made approximately 3 days before and approximately 6.5 hours after the infusion, whereas patients passively received tactile stimulation to the right and left index fingers and also while they rested (eyes-closed). Antidepressant response was assessed by percentage change in Montgomery-Åsberg Depression Rating Scale scores.
resultsPatients with robust improvements in depressive symptoms 230 min after infusion (responders) exhibited increased cortical excitability within this antidepressant response window. Specifically, we found that stimulus-evoked somatosensory cortical responses increase after infusion, relative to pretreatment responses in responders but not in treatment nonresponders. Spontaneous somatosensory cortical γ-band activity during rest did not change within the same timeframe after ketamine in either responders or nonresponders.
conclusionsThese findings suggest NMDAR antagonism does not lead directly to increased cortical excitability hours later and thus might not be sufficient for therapeutic effects of ketamine to take hold. Rather, increased cortical excitability as depressive symptoms improve is consistent with the hypothesis that enhanced non-NMDAR-mediated glutamatergic neurotransmission via synaptic potentiation is central to the antidepressant effect of ketamine.
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What 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.