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The beneficial effects of vortioxetine on BDNF, CREB, S100B, [beta] amyloid, and glutamate NR2b receptors in chronic unpredictable mild stress model of depression
Background Depression, one of the most significant mental disorders, is still poorly understood in terms of its pathogenetic mechanisms despite its well-recognized association with stress. Objectives The current study's goal was to ascertain how the novel antidepressant drug vortioxetine (VOR)...
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Published in: | Psychopharmacology 2023-12, Vol.240 (12), p.2499 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Background Depression, one of the most significant mental disorders, is still poorly understood in terms of its pathogenetic mechanisms despite its well-recognized association with stress. Objectives The current study's goal was to ascertain how the novel antidepressant drug vortioxetine (VOR) affected the BDNF (brain-derived neurotrophic factor), S100, amyloid [beta] (A[beta]), CREB (cAMP response element-binding protein), and NR2B, as well as its impact on depression-like behaviors, and tissue damage in an experimental rodent model of depression caused by chronic unpredictable stress. Methods We employed twenty-eight Wistar albino male rats, and we randomly divided them into four groups, each consisting of 7 rats: control, CUMS (chronic unpredictable mild stress), CUMS+vortioxetine (CUMS+VOR), and CUMS+fluoxetine (CUMS+FLU). Sucrose preference and forced swimming tests (SPT and FST, respectively), PCR, ELISA, and histopathological and immunohistochemical evaluation were made on brains. Results The behaviors of reduced immobility in the FST and increased sucrose preference were observed in the CUMS group and they improved in the groups treated with VOR and FLU. Compared with the control group, the group exposed to CUMS showed increased A[beta] and decreased BDNF, CREB, and S-100 expressions, as well as neuronal degeneration (p |
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ISSN: | 0033-3158 |
DOI: | 10.1007/s00213-023-06445-0 |