ArticlePsychopharmacology2015
Cell type-specific in vivo expression of genes encoding signalling molecules in the brain in response to chronic mild stress and chronic treatment with fluoxetine.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The Association Between Antidepressant Effect of SSRIs and Astrocytes: Conceptual Overview and Meta-analysis of the Literature.Neurochemical research · 2021Pooled it
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Astrocyte Ezrin defines resilience to stress-induced depressive behaviours in mice.National science review · 2026Article
- Major depressive disorder: hypothesis, mechanism, prevention and treatment.Signal transduction and targeted therapy · 2024Review
- Pathogenesis and therapeutic strategies for cancer-related depression.American journal of cancer research · 2024Review
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- A novel murine model of mania.Molecular psychiatry · 2023Article
- Electroacupuncture prevents astrocyte atrophy to alleviate depression.Cell death & disease · 2023Article
- Ketamine Alters Functional Plasticity of Astroglia: An Implication for Antidepressant Effect.Life (Basel, Switzerland) · 2021Review
- Ketamine Action on Astrocytes Provides New Insights into Rapid Antidepressant Mechanisms.Advances in neurobiology · 2021Review
- Astroglial Serotonin Receptors as the Central Target of Classic Antidepressants.Advances in neurobiology · 2021Article
- Chronic stress impairs the aquaporin-4-mediated glymphatic transport through glucocorticoid signaling.Psychopharmacology · 2019Article
- General Pathophysiology of Astroglia.Advances in experimental medicine and biology · 2019Review
- Sleep Disturbance in Bipolar Disorder: Neuroglia and Circadian Rhythms.Frontiers in psychiatry · 2019Review
- Leptin Increases Expression of 5-HTFrontiers in psychiatry · 2018Article
- Mechanism of depression as a risk factor in the development of Alzheimer's disease: the function of AQP4 and the glymphatic system.Psychopharmacology · 2017Article
- SSRI and Motor Recovery in Stroke: Reestablishment of Inhibitory Neural Network Tonus.Frontiers in neuroscience · 2017Article
- Translational potential of astrocytes in brain disorders.Progress in neurobiology · 2016Review
- Decrease of gene expression of astrocytic 5-HT2B receptors parallels development of depressive phenotype in a mouse model of Parkinson's disease.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationalePreviously, we reported that chronic treatment with fluoxetine increased gene expression of 5-hydroxytryptamine receptor 2B (5-HT2BR), cytosolic phospholipase 2α (cPLA2α), glutamate receptor, ionotropic kainate 2 (GluK2) and adenosine deaminase acting on RNA 2 (ADAR2), in cultured astrocytes and astrocytes freshly isolated from transgenic mice tagged with an astrocyte-specific marker. In contrast, neurones isolated from transgenic mice tagged with a neurone-specific marker and exposed to fluoxetine showed an increase in gene expression of glutamate receptor, ionotropic kainate 4 (GluK4) and 5-hydroxytryptamine receptor 2C (5-HT2CR). In a mouse model of anhedonia, the downregulation of 5-HT2BR, cPLA2α, ADAR2 and GluK4 but not GluK2 and 5-HT2CR was detected.
objectiveTo investigate the effects of chronic mild stress (CMS) and/or fluoxetine treatment on gene expression of 5-HT2BR, 5-HT2CR, cPLA2α, ADAR2, GluK2 and GluK4 specifically in astrocytes and neurones.
methodsTransgenic mice tagged with either astrocyte- or neurone-specific markers were exposed to the CMS. Real-time PCR was applied to determine expression of messenger RNA (mRNA).
resultsWe found that (i) mRNAs of the 5-HT2BR and cPLA2α in astrocytes and GluK4 in neurones were significantly reduced in mice that became anhedonic; the mRNA levels were restored by fluoxetine treatment; (ii) ADAR2 in astrocytes was decreased by the CMS but showed no response to fluoxetine in anhedonic animals; (iii) neither GluK2 expression in astrocytes nor 5-HT2CR expression in neurones were affected in anhedonic animals, although expression of 5-HT2CR mRNA was upregulated by fluoxetine.
conclusionsOur results indicate that the effects of chronic treatment with fluoxetine are not only dependent on the cell type studied but also on the development of anhedonia. This suggests that fluoxetine may affect major depression (MD) patients and healthy people in a different manner.
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