AI Article Synopsis
- Chronic treatment with antidepressants boosts neurogenesis in the hippocampus, but the specific molecular processes are not fully understood, with GSK-3β/β-catenin signaling emerging as a key player.
- Fluoxetine, a selective serotonin reuptake inhibitor, enhances the growth of neural precursor cells by increasing the phosphorylation of GSK-3β and levels of nuclear β-catenin, which promotes cell proliferation.
- The study finds that activating the 5-HT1A receptor is essential for fluoxetine's effects, as blocking this receptor diminishes the neurogenic response linked to the GSK-3β/β-catenin pathway.
Article Abstract
Background: It is generally accepted that chronic treatment with antidepressants increases hippocampal neurogenesis, but the molecular mechanisms underlying their effects are unknown. Recently, glycogen synthase kinase-3 beta (GSK-3β)/β-catenin signaling was shown to be involved in the mechanism of how antidepressants might influence hippocampal neurogenesis.
Methods: The aim of this study was to determine whether GSK-3β/β-catenin signaling is involved in the alteration of neurogenesis as a result of treatment with fluoxetine, a selective serotonin reuptake inhibitor. The mechanisms involved in fluoxetine's regulation of GSK-3β/β-catenin signaling pathway were also examined.
Results: Our results demonstrated that fluoxetine increased the proliferation of embryonic neural precursor cells (NPCs) by up-regulating the phosphorylation of Ser9 on GSK-3β and increasing the level of nuclear β-catenin. The overexpression of a stabilized β-catenin protein (ΔN89 β-catenin) significantly increased NPC proliferation, while inhibition of β-catenin expression in NPCs led to a significant decrease in the proliferation and reduced the proliferative effects induced by fluoxetine. The effects of fluoxetine-induced up-regulation of both phosphorylation of Ser9 on GSK-3β and nuclear β-catenin were significantly prevented by the 5-hydroxytryptamine-1A (5-HT1A) receptor antagonist WAY-100635.
Conclusions: The results demonstrate that fluoxetine may increase neurogenesis via the GSK-3β/β-catenin signaling pathway that links postsynaptic 5-HT1A receptor activation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376550 | PMC |
| http://dx.doi.org/10.1093/ijnp/pyu099 | DOI Listing |
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