ArticleJournal of psychiatric research2016
Evidence for alterations of the glial syncytial function in major depressive disorder.
Article in Journal of psychiatric research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Pooled it
- Evaluating Chronic Sex-Specific Changes in Glutamatergic Signaling Markers Following Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Cerebellar astrocytic alterations in depression.Translational psychiatry · 2026Article
- Aquaporin-4 Dysfunction in Depression: From Pathogenic Mechanisms to Novel Therapeutic Targeting.International journal of molecular sciences · 2026Review
- ATP Release Deficiency through Astrocytic Connexin 43 in the Dorsal Hippocampus Promotes Depressive- and Anxiety-Like Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Neuroanatomical substrates of perivascular space index: a morphometric and tractography study.Frontiers in psychiatry · 2026Article
- A Meta-Analysis of the Effects of Chronic Stress on the Prefrontal Transcriptome in Animal Models and Convergence with Existing Human Data.bioRxiv : the preprint server for biology · 2025Article
- Chronic Stress and Astrocyte Dysfunction in Depression: Molecular Mechanisms and Gene Expression Changes.Antioxidants (Basel, Switzerland) · 2025Review
- Stress-induced dysfunction of neurovascular astrocytes in the prefrontal cortex contributes to sex-dependent deficits in cognition and behavior.Molecular psychiatry · 2025Article
- When the Stars Misfire: Astrocytic Dysfunctions in Major Depressive Disorder.Neurochemical research · 2025Review
- Antidepressant effects of fluoxetine: upregulation of connexin 36 and 43 in the hippocampus, prefrontal cortex, and amygdala.Molecular biology reports · 2025Article
- Altered synaptic homeostasis: a key factor in the pathophysiology of depression.Cell & bioscience · 2025Review
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Biological, genetic, neurological and environmental influences on homosexuality-a narrative review.Frontiers in behavioral neuroscience · 2025Review
- Article
- Identification of Potential Biomarkers for Major Depressive Disorder: Based on Integrated Bioinformatics and Clinical Validation.Molecular neurobiology · 2024Article
- Reactive Astrocytosis-A Potential Contributor to Increased Suicide in Long COVID-19 Patients?Brain sciences · 2024Review
- Ketamine's mechanism of action with an emphasis on neuroimmune regulation: can the complement system complement ketamine's antidepressant effects?Molecular psychiatry · 2024Review
- Resource: A Curated Database of Brain-Related Functional Gene Sets (Brain.GMT).bioRxiv : the preprint server for biology · 2024Article
- Glymphatic System and Psychiatric Disorders: A Rapid Comprehensive Scoping Review.Current neuropharmacology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundGlial cells are essential in maintaining synaptic function. In glutamatergic synapses astrocytes remove the products of neural activity, (i.e. potassium, glutamate and excess water) from the synaptic cleft and redistribute them across the glial network; these products of neural activity can then be recycled for neuronal use or released into the vascular compartment. This type of highly coupled cell network -or syncytium-maintains the balance of synaptic activity by restoring the basal levels of such molecules in the synaptic cleft. Previous studies have reported alterations of glia related genes in Major Depressive Disorder, including some genes related to syncytial function.
methodsWe used RNA isolated from hippocampal tissues of 13 MDD subjects and 10 healthy controls to broadly examine gene expression using microarrays. Hippocampal RNA samples were isolated by laser capture microdissection from human tissue sections carefully avoiding contamination from neighboring structures. Once RNA quality was validated RNA was labeled and hybridized to microarrays.
resultsAnalysis of microarray data identified mRNA transcripts involved in glial syncytial function that were downregulated in MDD subjects compared to controls, including potassium and water channels (KCNJ10, AQP4), gap junction proteins (GJA1) and glutamate transporters (SLC1A2, SLC1A3). These gene expression differences were confirmed by qPCR.
conclusionsThe downregulation of these genes related to the syncytial network activity of glial cells is consistent with the hypothesis that synaptic homeostasis is disrupted thereby disrupting hippocampal synaptic function in MDD patients. Such glial gene expression changes could contribute either to the onset or perpetuation of depressive symptoms and hence, represent targets for novel therapeutics.
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Registered trials
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