ArticleBritish journal of pharmacology2003
Inhibition of G protein-activated inwardly rectifying K+ channels by fluoxetine (Prozac).
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 88 citations in OpenAlex.
- A randomized controlled study of the effect of ifenprodil on alcohol use in patients with alcohol dependence.Neuropsychopharmacology reports · 2018Trial
- The involvement of KTranslational psychiatry · 2024Review
- The Relevance of GIRK Channels in Heart Function.Membranes · 2022Review
- Review
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- GIRK2 Channels in Down Syndrome and Alzheimer's Disease.Current Alzheimer research · 2022Article
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- Advances in Targeting GIRK Channels in Disease.Trends in pharmacological sciences · 2021Review
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Chloroform is a potent activator of cardiac and neuronal Kir3 channels.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome.Neurobiology of disease · 2017Article
- The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome.Frontiers in cellular neuroscience · 2017Review
- Optical control of neuronal activity using a light-operated GIRK channel opener (LOGO).Chemical science · 2016Article
- Selective serotonin reuptake inhibitors facilitate ANO6 (TMEM16F) current activation and phosphatidylserine exposure.Pflugers Archiv : European journal of physiology · 2015Article
- Early-life serotonin dysregulation affects the migration and positioning of cortical interneuron subtypes.Translational psychiatry · 2015Article
- Interaction of paroxetine with mitochondrial proteins mediates neuroprotection.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Article
- Cardiac and renal inward rectifier potassium channel pharmacology: emerging tools for integrative physiology and therapeutics.Current opinion in pharmacology · 2014Review
- Review
- Kir6.2 is not the mitochondrial KATP channel but is required for cardioprotection by ischemic preconditioning.American journal of physiology. Heart and circulatory physiology · 2013Article
- Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel.Biochimica et biophysica acta · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of fluoxetine, a commonly used antidepressant drug, on G protein-activated inwardly rectifying K(+) channels (GIRK, Kir3) were investigated using Xenopus oocyte expression assays. 2. In oocytes injected with mRNAs for GIRK1/GIRK2, GIRK2 or GIRK1/GIRK4 subunits, fluoxetine reversibly reduced inward currents through the basal GIRK activity. The inhibition by fluoxetine showed a concentration-dependence, a weak voltage-dependence and a slight time-dependence with a predominant effect on the instantaneous current elicited by voltage pulses and followed by slight further inhibition. Furthermore, in oocytes expressing GIRK1/2 channels and the cloned Xenopus A(1) adenosine receptor, GIRK current responses activated by the receptor were inhibited by fluoxetine. In contrast, ROMK1 and IRK1 channels in other Kir channel subfamilies were insensitive to fluoxetine. 3. The inhibitory effect on GIRK channels was not obtained by intracellularly applied fluoxetine, and not affected by extracellular pH, which changed the proportion of the uncharged to protonated fluoxetine, suggesting that fluoxetine inhibits GIRK channels from the extracellular side. 4. The GIRK currents induced by ethanol were also attenuated in the presence of fluoxetine. 5. We demonstrate that fluoxetine, at low micromolar concentrations, inhibits GIRK channels that play an important role in the inhibitory regulation of neuronal excitability in most brain regions and the heart rate through activation of various G-protein-coupled receptors. The present results suggest that inhibition of GIRK channels by fluoxetine may contribute to some of its therapeutic effects and adverse side effects, particularly seizures in overdose, observed in clinical practice.
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