Abstract

Response: Commentary: Chronic SSRI Stimulation of Astrocytic 5-HT2B Receptors Change Multiple Gene Expressions/Editings and Metabolism of Glutamate, Glucose and Glycogen: A Potential Paradigm Shift.

Highlights

  • Stimulation by fluoxetine of the astrocytic 5-HT2B receptor causes a multitude of effects that in astrocyte cultures could be prevented by drug- or siRNA-induced 5-HT2B receptor inhibition (Figure 1)

  • Our studies in mice treated with fluoxetine for 2 weeks showed multiple gene upregulations and editings (Li et al, 2012; Hertz et al, 2015), which altered the function of the gene product in kainate receptors, 5-HT2 receptors, phospholipase cPLA2, a Ca2+ L-channel gene and nucleoside transporter genes

  • These changes occurred mainly in astrocytes but some were neuronal. They occurred together with effects on metabolism of glucose and glycogen and turnover of glutamate and GABA, consistent with evidence of increased glutamatergic activity and decreased GABA-ergic activity in patients suffering from major depression, which are reverted by successful therapy; glucose metabolism is decreased in depressed patients and increases following treatment (Hertz et al, 2015)

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Summary

Introduction

Commentary: Chronic SSRI stimulation of astrocytic 5-HT2B receptors change multiple gene expressions/editings and metabolism of glutamate, glucose and glycogen: a potential paradigm shift by Banas, S. Instead we pointed toward acute and chronic effects of fluoxetine on 5HT2B receptor stimulation in astrocytes (in culture or freshly isolated from brains of mice treated with fluoxetine for 14 days).

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