ReviewJournal of signal transduction2014
Signal Transduction in Astrocytes during Chronic or Acute Treatment with Drugs (SSRIs, Antibipolar Drugs, GABA-ergic Drugs, and Benzodiazepines) Ameliorating Mood Disorders.
Review in Journal of signal transduction, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The Association Between Antidepressant Effect of SSRIs and Astrocytes: Conceptual Overview and Meta-analysis of the Literature.Neurochemical research · 2021Pooled it
- Review
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Electroacupuncture prevents astrocyte atrophy to alleviate depression.Cell death & disease · 2023Article
- Astroglial Serotonin Receptors as the Central Target of Classic Antidepressants.Advances in neurobiology · 2021Article
- Luteolin Modulates Neural Stem Cells Fate Determination:Frontiers in cell and developmental biology · 2021Article
- Reduced uptake of [11C]-ABP688, a PET tracer for metabolic glutamate receptor 5 in hippocampus and amygdala in Alzheimer's dementia.Brain and behavior · 2020Article
- Diverse Actions of Astrocytes in GABAergic Signaling.International journal of molecular sciences · 2019Review
- Mechanism of depression as a risk factor in the development of Alzheimer's disease: the function of AQP4 and the glymphatic system.Psychopharmacology · 2017Article
- Biphasic Regulation of Caveolin-1 Gene Expression by Fluoxetine in Astrocytes: Opposite Effects of PI3K/AKT and MAPK/ERK Signaling Pathways on c-fos.Frontiers in cellular neuroscience · 2017Article
- Astrocyte Cultures Mimicking Brain Astrocytes in Gene Expression, Signaling, Metabolism and KNeurochemical research · 2017Article
- Understanding epigenetic architecture of suicide neurobiology: A critical perspective.Neuroscience and biobehavioral reviews · 2017Review
- Astrocytes in Oligodendrocyte Lineage Development and White Matter Pathology.Frontiers in cellular neuroscience · 2016Review
- 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.Psychopharmacology · 2015Article
- Astrocytic glycogenolysis: mechanisms and functions.Metabolic brain disease · 2015Review
- Reduced density of glutamine synthetase immunoreactive astrocytes in different cortical areas in major depression but not in bipolar I disorder.Frontiers in cellular neuroscience · 2015Article
- Chronic SSRI stimulation of astrocytic 5-HT2B receptors change multiple gene expressions/editings and metabolism of glutamate, glucose and glycogen: a potential paradigm shift.Frontiers in behavioral neuroscience · 2015Review
- Fluoxetine and all other SSRIs are 5-HT2B Agonists - Importance for their Therapeutic Effects.Current neuropharmacology · 2014Article
- Basic mechanism leading to stimulation of glycogenolysis by isoproterenol, EGF, elevated extracellular K+ concentrations, or GABA.Neurochemical research · 2014Article
- Inhibition of brain swelling after ischemia-reperfusion by β-adrenergic antagonists: correlation with increased K+ and decreased Ca2+ concentrations in extracellular fluid.BioMed research international · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic treatment with fluoxetine or other so-called serotonin-specific reuptake inhibitor antidepressants (SSRIs) or with a lithium salt "lithium", carbamazepine, or valproic acid, the three classical antibipolar drugs, exerts a multitude of effects on astrocytes, which in turn modulate astrocyte-neuronal interactions and brain function. In the case of the SSRIs, they are to a large extent due to 5-HT2B-mediated upregulation and editing of genes. These alterations induce alteration in effects of cPLA2, GluK2, and the 5-HT2B receptor, probably including increases in both glucose metabolism and glycogen turnover, which in combination have therapeutic effect on major depression. The ability of increased levels of extracellular K(+) to increase [Ca(2+)] i is increased as a sign of increased K(+)-induced excitability in astrocytes. Acute anxiolytic drug treatment with benzodiazepines or GABAA receptor stimulation has similar glycogenolysis-enhancing effects. The antibipolar drugs induce intracellular alkalinization in astrocytes with lithium acting on one acid extruder and carbamazepine and valproic acid on a different acid extruder. They inhibit K(+)-induced and transmitter-induced increase of astrocytic [Ca(2+)] i and thereby probably excitability. In several cases, they exert different changes in gene expression than SSRIs, determined both in cultured astrocytes and in freshly isolated astrocytes from drug-treated animals.
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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.