Effects of fluvoxamine on nerve growth factor-induced neurite outgrowth inhibition by dexamethasone in PC12 cells. Issue 4 (3rd April 2019)

• Record Type: Journal Article
• Authors: Matsushima, Yukari; Terada, Kazuki; Takata, Jiro; Karube, Yoshiharu; Kamei, Chiaki; Sugimoto, Yumi
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 83:Issue 4(2019)
• Page Start: 659
• Page End: 665
• Publication Date: 2019-04-03
• Subjects: Nerve growth factor (NGF) -- neurite outgrowth -- fluvoxamine -- phosphorylated Akt -- dexamethasone (DEX); Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2018.1553607
• Languages: English
• ISSNs: 0916-8451

Abstract

ABSTRACT: In the present study, we examined the effects of fluvoxamine on nerve growth factor (NGF)-induced neurite outgrowth inhibition by dexamethasone (DEX) in PC12 cells. Fluvoxamine increased NGF-induced neurite outgrowth. Compared with co-treatment with NGF and fluvoxamine, p-Akt levels were higher than the values without fluvoxamine. The phosphorylated extracellular regulated kinase 1/2 levels were slightly increased by co-treatment with NGF and fluvoxamine. Fluvoxamine concentration-dependently improved NGF-induced neurite outgrowth inhibition by DEX. Fluvoxamine also improved the decrease in the NGF-induced p-Akt level caused by DEX. Interestingly, the sigma-1 receptor antagonist NE-100 blocked the improvement effects of fluvoxamine on NGF-induced neurite outgrowth inhibition by DEX. The selective sigma-1 receptor agonist PRE-084 also improved NGF-induced neurite outgrowth inhibition by DEX, which is blocked by NE-100. These results indicate that the improvement effects of fluvoxamine on NGF-induced neurite outgrowth inhibition by DEX may be attributable to the phosphorylation of Akt and the sigma-1 receptor. Graphical abstract: : Fluvoxamine improved NGF-induced neurite outgrowth inhibition by DEX.