ArticlePsychopharmacology2011
Fluoxetine attenuates the inhibitory effect of glucocorticoid hormones on neurogenesis in vitro via a two-pore domain potassium channel, TREK-1.
Article in Psychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Metabolomics in Depression: What We Learn from Preclinical and Clinical Evidences.Molecular neurobiology · 2025Pooled it
- Gut microbial metabolite TMAO impairs cognitive function and induces hippocampal synaptic plasticity decline through modulation of GSK-3β activity.Alzheimer's research & therapy · 2025Article
- Tick-Derived Peptide Blocks Potassium Channel TREK-1.International journal of molecular sciences · 2024Article
- Review
- The Two-Pore Domain Potassium Channel TREK-1 Promotes Blood-Brain Barrier Breakdown and Exacerbates Neuronal Death After Focal Cerebral Ischemia in Mice.Molecular neurobiology · 2022Article
- Article
- The Lectin LecA Sensitizes the Human Stretch-Activated Channel TREK-1 but Not Piezo1 and Binds Selectively to Cardiac Non-myocytes.Frontiers in physiology · 2020Article
- The involvement of potassium channel ORK1 in short-term memory and sleep in Drosophila.Medicine · 2017Article
- Over-expressed human TREK-1 inhibits CHO cell proliferation via inhibiting PKA and p38 MAPK pathways and subsequently inducing G1 arrest.Acta pharmacologica Sinica · 2016Article
- The Current Situation on Major Depressive Disorder in China: Research on Mechanisms and Clinical Practice.Neuroscience bulletin · 2016Review
- Effects of neonatal stress on gamma oscillations in hippocampus.Scientific reports · 2016Article
- A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives.BioMed research international · 2016Review
- Potentiation of Schaffer-Collateral CA1 Synaptic Transmission by eEF2K and p38 MAPK Mediated Mechanisms.Frontiers in cellular neuroscience · 2016Article
- Article
- The Role of the Two-Pore Domain Potassium Channel TREK-1 in the Therapeutic Effects of Escitalopram in a Rat Model of Poststroke Depression.CNS neuroscience & therapeutics · 2015Article
- The role of K₂p channels in anaesthesia and sleep.Pflugers Archiv : European journal of physiology · 2015Review
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
- Effects of fluoxetine on protein expression of potassium ion channels in the brain of chronic mild stress rats.Acta pharmaceutica Sinica. B · 2015Article
- Stress, glucocorticoid hormones, and hippocampal neural progenitor cells: implications to mood disorders.Frontiers in physiology · 2015Review
- Fluoxetine regulates neurogenesis in vitro through modulation of GSK-3β/β-catenin signaling.The international journal of neuropsychopharmacology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleSustained stress and elevated glucocorticoid reduces neurogenesis, whereas chronic treatment with antidepressants increases neurogenesis and blocks the effects of stress. Recently, TREK-1, a two-pore domain (K(2)p) potassium channel, has been shown to be involved in the mechanisms of major depression.
objectivesThis study aimed to investigate whether TREK-1 is involved in the alteration of neurogenesis according to glucocorticoids and antidepressants.
resultsThe present study addressed the expression of TREK-1 in neural stem cells (NSCs) and found TREK-1 was only associated with NSC proliferation. Bupivacaine and curcumin, two strong TREK-1 channel inhibitors, significantly increased embryonic NSC viability and proliferation while transfection of hTREK-1 decreased cell proliferation in embryonic NSCs. Dexamethasone, a glucocorticoid hormone receptor agonist, upregulated both protein and mRNA levels of TREK-1 leading to decreased NSC proliferation which could be reversed by bupivacaine. Fluoxetine, a serotonin reuptake inhibitor antidepressant that has been previously found to inhibit TREK-1 channels, robustly, could attenuate the upregulation of TREK-1 expression and the inhibition of NSC proliferation induced by dexamethasone.
conclusionsTaken together, these data suggest that TREK-1 is associated with NSC proliferation and probably is a modulator of the effect that fluoxetine attenuates the inhibitory neurogenesis induced by glucocorticoid hormones.
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