ReviewMolecular psychiatry2018
Engaging homeostatic plasticity to treat depression.
Review in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 43 citations in OpenAlex.
- Maladaptive Neuroplasticity Under Stress: Insights into Neuronal and Synaptic Changes in the Prefrontal Cortex.Molecular neurobiology · 2025Review
- Retinoid homeostasis in major depressive disorder.Translational psychiatry · 2023Article
- Neural activations to loss anticipation mediates the association between difficulties in emotion regulation and screen media activities among early adolescent youth: A moderating role for depression.Developmental cognitive neuroscience · 2022Article
- Acute Ketamine Facilitates Fear Memory Extinction in a Rat Model of PTSD Along With Restoring Glutamatergic Alterations and Dendritic Atrophy in the Prefrontal Cortex.Frontiers in pharmacology · 2022Article
- Role of FMRP in rapid antidepressant effects and synapse regulation.Molecular psychiatry · 2021Article
- Ketamine-50 years in use: from anesthesia to rapid antidepressant effects and neurobiological mechanisms.Pharmacological reports : PR · 2021Review
- Hallucinogens in Mental Health: Preclinical and Clinical Studies on LSD, Psilocybin, MDMA, and Ketamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Article
- Decreased Plasma Hydrogen Sulfide Level Is Associated With the Severity of Depression in Patients With Depressive Disorder.Frontiers in psychiatry · 2021Article
- Uncovering the Underlying Mechanisms of Ketamine as a Novel Antidepressant.Frontiers in pharmacology · 2021Review
- Cerebrospinal fluid neuroplasticity-associated protein levels in patients with psychiatric disorders: a multiplex immunoassay study.Translational psychiatry · 2020Article
- Protein Translation and Psychiatric Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Cortical Excitability and Activation of TrkB Signaling During Rebound Slow Oscillations Are Critical for Rapid Antidepressant Responses.Molecular neurobiology · 2019Article
- Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF trafficking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine.Neurobiology of stress · 2019Article
- Glutamatergic Neurotransmission: Pathway to Developing Novel Rapid-Acting Antidepressant Treatments.The international journal of neuropsychopharmacology · 2019Review
- Ketamine administration during a critical period after forced ethanol abstinence inhibits the development of time-dependent affective disturbances.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Hyperforin Potentiates Antidepressant-Like Activity of Lanicemine in Mice.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Major depressive disorder (MDD) is a complex and heterogeneous mood disorder, making it difficult to develop a generalized, pharmacological therapy that is effective for all who suffer from MDD. Through the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as effective antidepressants, we have gained key insights into how antidepressant effects can be produced at the circuit and molecular levels. NMDAR antagonists act as rapid-acting antidepressants such that relief from depressive symptoms occurs within hours of a single injection. The mode of action of NMDAR antagonists seemingly relies on their ability to activate protein-synthesis-dependent homeostatic mechanisms that restore top-down excitatory connections. Recent evidence suggests that NMDAR antagonists relieve depressive symptoms by forming new synapses resulting in increased excitatory drive. This event requires the mammalian target of rapamycin complex 1 (mTORC1), a signaling pathway that regulates synaptic protein synthesis. Herein, we review critical studies that shed light on the action of NMDAR antagonists as rapid-acting antidepressants and how they engage a neuron's or neural network's homeostatic mechanisms to self-correct. Recent studies notably demonstrate that a shift in γ-amino-butyric acid receptor B (GABA
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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.