ReviewNeuroscience letters2015
Spine synapse remodeling in the pathophysiology and treatment of depression.
Review in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 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
125 citing papers in PubMed, 266 citations in OpenAlex.
- Ketamine metabolite pilot study in a suicidal depression trial.Journal of psychiatric research · 2019Trial
- Aberrant expression of long non-coding RNAs and their regulatory role in chromatin-mediated gene expression changes in the prefrontal cortex of major depressive disorder subjects.Molecular psychiatry · 2026Article
- In Vivo Positron Emission Tomography Imaging of Presynaptic Density Reveals Stress-Associated Synaptic Deficits Related to Behavioral and Molecular Alterations in Rats.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2026Article
- Hippocampal subfield-specific imaging in depression: the translational power of ultra-high field MRI.Translational psychiatry · 2026Review
- Prefrontal spine loss in neuropsychiatric disorders: circuit consequences for cognition.Frontiers in psychiatry · 2026Review
- Stress-Induced Dysregulation of the Guidance Cue Receptor DCC Alters Corticolimbic Circuit Architecture.Biological psychiatry global open science · 2026Article
- Stress-Associated Changes in MiR-20b-3p as a Potential Predictor of Underlying Psychopathology in the Depressed Brain: Mechanistic Insights from a Rat Model of Chronic Restraint Stress.Molecular neurobiology · 2025Article
- Bioinformatics Analysis of Persistent Dysregulated Expression of Genes Involved in HCV-Induced Neurological Disorders and Liver Injuries After DAA Treatment Through Weighted Gene Co-Expression Network Analysis.Health science reports · 2025Article
- Analysis of the Correlation Between Depression-like Behaviors and Lipid Peroxidation in the Prefrontal Cortex of Mice: The Impact of Early Life Stress.Brain sciences · 2025Article
- Shared Mechanisms in Dementia and Depression: The Modulatory Role of Physical Exercise.Journal of neurochemistry · 2025Review
- Sex-Specific Neuropsychiatric Effects of Subanesthetic Ketamine Exposure in Pregnant Mice and Their Offspring.Cellular and molecular neurobiology · 2025Article
- Sensory neurostimulation promotes stress resilience with frequency-specificity.bioRxiv : the preprint server for biology · 2025Article
- Environmental determinants of ketamine's prohedonic and antianhedonic efficacy: Persistence of enhanced reward responsiveness is modulated by chronic stress.The Journal of pharmacology and experimental therapeutics · 2025Article
- Npbwr1 signaling mediates fast antidepressant action.Molecular psychiatry · 2025Article
- Effects of Qingyangshen glycosides on neuroplasticity in a mouse model of social defeat.Animal models and experimental medicine · 2025Article
- Monoamine-Uptake Inhibitors and Pain: Antidepressant Drugs Among First-Line Treatments Against Neuropathic Pain and Fibromyalgia.Advances in neurobiology · 2025Review
- Cocaine-Induced Microglial Impairment and Its Rehabilitation by PLX-PAD Cell Therapy.International journal of molecular sciences · 2024Article
- Complement and microglia activation mediate stress-induced synapse loss in layer 2/3 of the medial prefrontal cortex in male mice.Nature communications · 2024Article
- Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Ketamine's mechanism of action with an emphasis on neuroimmune regulation: can the complement system complement ketamine's antidepressant effects?Molecular psychiatry · 2024Review
65 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Clinical brain imaging and postmortem studies provide evidence of structural and functional abnormalities of key limbic and cortical structures in depressed patients, suggesting that spine synapse connectivity is altered in depression. Characterization of the cellular determinants underlying these changes in patients are limited, but studies in rodent models demonstrate alterations of dendrite complexity and spine density and function that could contribute to the morphological and functional alterations observed in humans. Rodent studies demonstrate region specific effects in chronic stress models of depression, including reductions in dendrite complexity and spine density in the hippocampus and prefrontal cortex (PFC) but increases in the basolateral amygdala and nucleus accumbens. Alterations of spine synapse connectivity in these regions are thought to contribute to the behavioral symptoms of depression, including disruption of cognition, mood, emotion, motivation, and reward. Studies of the mechanisms underlying these effects demonstrate a role for altered brain derived neurotrophic factor (BDNF) signaling that regulates synaptic protein synthesis. In contrast, there is evidence that chronic antidepressant treatment can block or reverse the spine synapse alterations caused by stress. Notably, the new fast acting antidepressant ketamine, which produces rapid therapeutic actions in treatment resistant MDD patients, rapidly increases spine synapse number in the PFC of rodents and reverses the effects of chronic stress. The rapid synaptic and behavioral actions of ketamine occur via increased BDNF regulation of synaptic protein synthesis. Together these studies provide evidence for a neurotophic and synaptogenic hypothesis of depression and treatment response and indicate that spine synapse connectivity in key cortical and limbic brain regions is critical for control of mood and emotion.
Indexed as
Identifiers
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.