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. 2018 Oct 24;19(11):3313. doi: 10.3390/ijms19113313

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Non-monoaminergic mechanism underlying the antidepressant action of fluoxetine via astrocytic brain-derived neurotrophic factor (BDNF) expression and reported Kir4.1 channel blockers. In silico docking model analysis of Kir4.1 channels with antidepressant drugs revealed that Glu158 can interact with the amine moiety of fluoxetine with an ionic bond and Thr128 with the benzene ring (hydrogen bond acceptor) with a hydrogen bond. The blockade of Kir4.1 channels by fluoxetine facilitate a BDNF mRNA and protein expression in astrocytes, which can potentially alleviate depressive disorders by enhancing neural plasticity, neurogenesis, and survival of 5-HT and noradrenaline (NA) neurons. Kir4.1 channel blockers currently reported are shown in a right side panel. SSRI: Selective serotonin reuptake inhibitor. TCA: Tricyclic antidepressants.