A role for nuclear β-catenin in SNRI antidepressant-induced hippocampal cell proliferation

Mostany, Ricardo; Valdizán, Elsa M.; Pazos, Angel

doi:10.1016/j.neuropharm.2008.04.012

Cited by 47Neurogenesis and neuroplasticity mechanismsTreatment of Major DepressionNeuroscience and Neuropharmacology Research

A role for nuclear β-catenin in SNRI antidepressant-induced hippocampal cell proliferation

Mostany, Ricardo, Valdizán, Elsa M., Pazos, Angel·2008·Neuropharmacology

DOI 10.1016/j.neuropharm.2008.04.012

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Abstract

Increasing evidences have been accumulated during recent years suggesting a role for antidepressant drugs (ADs) as hippocampal neurogenesis enhancers, but the information about the transductional mechanisms involved in this response is very limited. We have studied in the adult rat hippocampus the effects of chronic treatment with the dual reuptake inhibitor (SNRI) venlafaxine on both cellular proliferation rate and expression of key effectors of several signaling pathways. Increased cell proliferation (BrdU incorporation) in subgranular zone (SGZ) was achieved after chronic treatment with a high dose (40 mg/kg/day) of venlafaxine. However, significant increases in the immunoreactivity of hippocampal beta-catenin in SGZ were already detected after administration of a lower dose of the drug (10 mg/kg/day). Western blot and immunoelectron microscopy studies demonstrated an increased presence of beta-catenin at the nuclear level. An increase in cytosolic AKT levels was also observed in venlafaxine-treated animals. These results suggest that the hippocampal proliferative effect of chronic venlafaxine, only evident when both serotonin (5-HT) and noradrenaline/norepinephrine (NE) reuptake systems are inhibited, requires a strong activation of intracellular signaling through Wnt (beta-catenin translocation) and AKT/PKB pathways. This activation would probably result in an increase of the expression of cell cycle regulator genes. Furthermore pERK2/ERK2 rate was also increased in the hippocampus of AD-treated animals, while no differences in the levels of CREB and p-CREB were observed. These results illustrate the complexity of the intracellular events underlying the neurogenetic responses of ADs. They also support the relevance of such effects for the therapeutic effects of these drugs.

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Antidepressant treatment produces increased Akt levels in several brain structures, including the hippocampus and prefrontal cortex.
“AD also produces increased Akt levels in several brain structures, including the hippocampus [18] and prefrontal cortex [15].”
From The Impact of BDNF, NTRK2, NGFR, CREB1, GSK3B, AKT, MAPK1, MTOR, PTEN, ARC, and SYN1 Genetic Polymorphisms in Antidepressant Treatment Response Phenotypes (2023) · cites this paper as [18]

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Authors: Mostany, R., Valdizán, E. M., & Pazos, A.
Affiliations: Universidad de Cantabria (ES)
ORCID: Mostany, Ricardo
Valdizán, Elsa M.
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 2008-07
Volume: 55
Issue: 1
Pages: 18-26
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/j.neuropharm.2008.04.012
OpenAlex: W2089141291
Cited by: 47
References: 57
Citations by year: 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2019: 2 · 2018: 6 · 2017: 1 · 2016: 4 · 2015: 2 · 2014: 4 · 2013: 6 · 2012: 1
FWCI: 1.11
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Topics: Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: venlafaxine, selective serotonin reuptake inhibitors, antidepressants, hippocampal neurogenesis, hippocampal cell proliferation, subgranular zone, nuclear β-catenin, Wnt signaling, ERK2 phosphorylation, CREB, serotonin reuptake inhibition, norepinephrine reuptake inhibition, chronic drug administration
MeSH terms: Venlafaxine Hydrochloride, Animals, Antidepressive Agents, Bromodeoxyuridine, Cell Nucleus, Cyclohexanols, Dose-Response Relationship, Drug, Gene Expression Regulation, Hippocampus, Male, Microscopy, Electron, Models, Biological, Neurons, Subcellular Fractions, Signal Transduction, Rats, Wistar, Cell Proliferation, beta Catenin, Rats

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