Behavioural and neuroplastic effects of the new-generation antidepressant agomelatine compared to fluoxetine in glucocorticoid receptor-impaired mice
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Major depression is associated with reduced hippocampal volume linked to stress and high glucocorticoid secretion. Glucocorticoid receptor-impaired (GR-i) mice, a transgenic model for affective disorders with hypothalamic-pituitary-adrenal (HPA) axis feedback control deficit, were used to assess the antidepressant-like effects of the mixed melatonin receptor agonist/5-HT(2C) receptor antagonist, agomelatine, compared to the selective 5-HT reuptake inhibitor (SSRI), fluoxetine, on hippocampal neurogenesis, GR and BDNF expression and antidepressant-responsive behaviour (tail suspension test, TST). GR-i and paired wild-type (WT) mice were given acute or chronic (21 d) treatment with these drugs. Both hippocampal cell proliferation and BDNF mRNA expression were down-regulated in GR-i mice, and these alterations were reversed by chronic agomelatine and fluoxetine treatments, whereas GR mRNA down-regulation was reversed only by agomelatine. Furthermore, chronic agomelatine, but not fluoxetine, increased survival of newly formed cells in the ventral part of the hippocampus without changing their phenotypic differentiation into neurons. In the TST, the enhanced immobility of GR-i mice was reduced to WT level by acute (but not chronic) fluoxetine and chronic (but not acute) agomelatine. These results indicate that agomelatine reversed the neuroplastic changes and helpless behaviour associated with HPA axis alterations in GR-i mice, suggesting neurobiological and behavioural effects mostly similar to those typically seen with classical antidepressants such as fluoxetine, but through clearly distinct mechanisms.
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In preclinical depression-like models, impaired neurogenesis is observed in rodent models of depressive-like behavior.
“Hence, using proliferation and survival cell markers such as BrdU, Ki-67, or DCX, impaired neurogenesis was observed in rodent models of depressive-like behavior.”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Paizanis et al. 2010
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- Authors
- Païzanis, E., Renoir, T., Lelievre, V., Saurini, F., Melfort, M., Gabriel, C., Barden, N., Mocaër, E., Hamon, M., & Lanfumey, L.
- Affiliations
- Inserm (FR)
- Institut de Relations Internationales et Stratégiques (FR)
- Centre hospitalier de l'Université Laval (CA)
- Corresponding author
- Lanfumey, Laurence
- Venue
- The International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-09-24
- Volume
- 13
- Issue
- 06
- Pages
- 759-774
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- OpenAlex
- W2003762546
- Cited by
- 123
- References
- 69
- Citations by year
- 2024: 1 · 2023: 5 · 2022: 6 · 2021: 3 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 8 · 2015: 4 · 2014: 13 · 2013: 17 · 2012: 16
- FWCI
- 11.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Eli Lilly and Company
- Institut National de la Santé et de la Recherche Médicale
- Centre National de la Recherche Scientifique
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- agomelatine, fluoxetine, major depressive disorder, hippocampal neurogenesis, brain-derived neurotrophic factor, glucocorticoid receptor, hypothalamic-pituitary-adrenal axis, antidepressant-like effects, tail suspension test, neuroplasticity, melatonin receptor agonists, 5-HT2C receptor antagonist, selective serotonin reuptake inhibitors
- MeSH terms
- Acetamides, Doublecortin Domain Proteins, Animals, Antidepressive Agents, Behavior, Animal, Bromodeoxyuridine, Drug Administration Schedule, Fluoxetine, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Hippocampus, Male, Mice, Transgenic, Microtubule-Associated Proteins, Naphthalenes, Neuronal Plasticity, Neuropeptides, Receptors, Glucocorticoid, RNA, Messenger, Cell Death, Brain-Derived Neurotrophic Factor, Hindlimb Suspension, In Situ Nick-End Labeling, Cell Proliferation, Mice, Rats
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