ReviewCNS spectrums2013
Second messenger/signal transduction pathways in major mood disorders: moving from membrane to mechanism of action, part I: major depressive disorder.
Review in CNS spectrums, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 43 citations in OpenAlex.
- Ketamine's antidepressant efficacy is extended for at least four weeks in subjects with a family history of an alcohol use disorder.The international journal of neuropsychopharmacology · 2014Trial
- Clinical predictors of ketamine response in treatment-resistant major depression.The Journal of clinical psychiatry · 2014Trial
- Persistent and Dose-Dependent Neural and Metabolic Gene Expression Changes Induced by Transient Citalopram Exposure in Zebrafish Embryos.International journal of molecular sciences · 2025Article
- Abnormal choroid plexus, hippocampus, and lateral ventricles volumes as markers of treatment-resistant major depressive disorder.Psychiatry and clinical neurosciences · 2025Article
- Review
- Two polygenic mouse models of major depressive disorders identify TMEM161B as a potential biomarker of disease in humans.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Molecular basis and mechanism of action ofChinese herbal medicines · 2023Review
- Alpha-Asarone modulates kynurenine disposal in muscle and mediates resilience to stress-induced depression via PGC-1α induction.CNS neuroscience & therapeutics · 2023Article
- Insights into the Promising Prospect of G Protein and GPCR-Mediated Signaling in Neuropathophysiology and Its Therapeutic Regulation.Oxidative medicine and cellular longevity · 2022Review
- Lithium as a Neuroprotective Agent for Bipolar Disorder: An Overview.Cellular and molecular neurobiology · 2022Review
- miR-323a regulates ERBB4 and is involved in depression.Molecular psychiatry · 2021Article
- An integrative network analysis framework for identifying molecular functions in complex disorders examining major depressive disorder as a test case.Scientific reports · 2021Article
- Behavioral and Neuroanatomical Consequences of Cell-Type Specific Loss of Dopamine D2 Receptors in the Mouse Cerebral Cortex.Frontiers in behavioral neuroscience · 2021Article
- Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice.Translational psychiatry · 2020Article
- Integrated Metabolomics and Proteomics Analysis Revealed Second Messenger System Disturbance in Hippocampus of Chronic Social Defeat Stress Rat.Frontiers in neuroscience · 2019Article
- Modulation of PKA, PKC, CAMKII, ERK 1/2 pathways is involved in the acute antidepressant-like effect of (octylseleno)-xylofuranoside (OSX) in mice.Psychopharmacology · 2017Article
- Article
- Genetic overlap between type 2 diabetes and major depressive disorder identified by bioinformatics analysis.Oncotarget · 2016Article
- Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice.The Journal of biological chemistry · 2015Article
- Ketamine and other N-methyl-D-aspartate receptor antagonists in the treatment of depression: a perspective review.Therapeutic advances in chronic disease · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The etiopathogenesis and treatment of major mood disorders have historically focused on modulation of monoaminergic (serotonin, norepinephrine, dopamine) and amino acid [γ-aminobutyric acid (GABA), glutamate] receptors at the plasma membrane. Although the activation and inhibition of these receptors acutely alter local neurotransmitter levels, their neuropsychiatric effects are not immediately observed. This time lag implicates intracellular neuroplasticity as primary in the mechanism of action of antidepressants and mood stabilizers. The modulation of intracellular second messenger/signal transduction cascades affects neurotrophic pathways that are both necessary and sufficient for monoaminergic and amino acid-based treatments. In this review, we will discuss the evidence in support of intracellular mediators in the pathophysiology and treatment of preclinical models of despair and major depressive disorder (MDD). More specifically, we will focus on the following pathways: cAMP/PKA/CREB, neurotrophin-mediated (MAPK and others), p11, Wnt/Fz/Dvl/GSK3β, and NFκB/ΔFosB. We will also discuss recent discoveries with rapidly acting antidepressants, which activate the mammalian target of rapamycin (mTOR) and release of inhibition on local translation via elongation factor stimulation. Throughout this discourse, we will highlight potential intracellular targets for therapeutic intervention. Finally, future clinical implications are discussed.
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What Socratic 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 Socratic graph.