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The mood-improving actions of antidepressants do not depend on neurogenesis but are associated with neuronal remodeling
Open accessAbstract
The mechanisms underlying the initiation/onset of, and the recovery from, depression are still largely unknown; views that neurogenesis in the hippocampus may be important for the pathogenesis and amelioration of depressive symptoms have gained currency over the years although the original evidence has been challenged. In this study, an unpredictable chronic mild stress protocol was used to induce a depressive-like phenotype in rats. In the last 2 weeks of stress exposure, animals were treated with the antidepressants fluoxetine, imipramine, CP 156,526 or SSR 1494515, alone or combined with methylazoxymethanol, a cytostatic agent used to arrest neurogenesis. We found that antidepressants retain their therapeutic efficacy in reducing both measured indices of depression-like behavior (learned helplessness and anhedonia), even when neurogenesis is blocked. Instead, our experiments suggest re-establishment of neuronal plasticity (dendritic remodeling and synaptic contacts) in the hippocampus and prefrontal cortex, rather than neurogenesis, as the basis for the restoration of behavioral homeostasis by antidepressants.
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“In summary, the results of several experiments indicated very clearly that in rodents undergoing chronic mild stress or stress induced by corticosterone and whose neurogenesis has been ablated, some behavioral depression-like signs are ameliorated independently of neurogenesis, while some others are dependent (Airan et al., 2007;Bessa et al., 2009;Surget et al., 2008;David et al., 2009).”
From Depression and adult neurogenesis: Positive effects of the antidepressant fluoxetine and of physical exercise (2018) · cites this paper as Bessa et al., 2009
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In the citing paper
“Furthermore, mounting evidence seems to indicate that neurogenesis might not be required for the therapeutic action of antidepressants (Bessa et al. 2009).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Bessa et al. 2009
In the citing paper
“Chronic, but not acute, administration of conventional antidepressants also reverses stress-induced dendritic atrophy in rodents[126]”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [126]
In the citing paper
“The sample sizes were based on previous published studies.9, 20”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“at short-term, behavioral improvements induced by ADs rely on hippocampal neuronal remodeling,9”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“Rats were subjected to a validated uCMS protocol for 6 weeks, as previously described9, 20, 23”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“in line with previous studies demonstrating that ADs, including imipramine, reverse the shrinkage in dendritic branching induced by stress and allows the re-establishment of the normal neuronal network,9”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“Besides boosting adult neurogenesis, fluoxetine treatment and further stress re-exposure also induced dendritic atrophy of the DG granule neurons, similar to the immediate effects induced by uCMS protocol in non-treated animals.9”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“These residual changes, together with reported impairments in DG synaptic plasticity9, 28, 29 may account for the re-appearance of depressive, anxiety and cognitive deficits on uCMS re-exposure.”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [9]
In the citing paper
“In rodents, exposure to protocol of chronic stressors, that modeling some features of psychiatric disorders symptoms, induce alterations in dendritic remodeling and decrease adult hippocampal neurogenesis (38, 44, 99).”
From Translational investigation of the therapeutic potential of Cannabidiol (CBD): Toward a new age (2018) · cites this paper as [99]
In the citing paper
“Other studies have concluded that long-term use of antidepressants can increase spine density or decrease atrophy of spines and dendrites after chronic stress.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [48]
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Malfunction in GABA and Glutamate as Pathways to Depression: A Review of the Evidence
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Miranda, A., Roque, S., Serre-Miranda, C., Pêgo, J. M., & Correia‐Pinto, J. (2017) · Journal of Pediatric Surgery · doi:10.1016/j.jpedsurg.2017.08.016 · Cited by 5
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“12,14 In human, neuroimaging evidence supports a normalization of the prefrontal cortex dysfunction in those MDD/TRD subject that responds to any antidepressant treatment.”
BackgroundKrishna, V., Nayak, V., Pandey, A. K., Sunny, S. V., & Bairy, K. L. (2021) · Research Journal of Pharmacy and Technology · doi:10.52711/0974-360x.2021.00333 · Cited by 5
Loureiro‐Campos, E., Mateus-Pinheiro, A., Patrício, P., Soares‐Cunha, C., Silva, J., Sardinha, V. M., Mendes-Pinheiro, B., Silveira‐Rosa, T., Domingues, A. V., Rodrigues, A. J., et al. (2021) · eLife · doi:10.7554/elife.70685 · Cited by 5
Self-citationČulig, L., & Belzung, C. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-801977-1.00009-x · Cited by 6
Bolzan, J. A., Martins, T., Domingues, K., Surget, A., Belzung, C., & de Oliveira, C. L. (2025) · Journal of Psychopharmacology · doi:10.1177/02698811251337382 · Cited by 6
Koehl, M., Ladevèze, E., Montcouquiol, M., & Abrous, D. N. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.844255 · Cited by 4
La kétamine : un neuropsychotrope au mécanisme d’action innovant
Guilloux, J., Nguyen, T. M. L., & Gardier, A. M. (2023) · Biologie Aujourd hui · doi:10.1051/jbio/2023026 · Cited by 5
Ketamine’s Mechanism of Rapid Antidepressant Activity: Evidence Gleaned from Clinical Studies
Averill, L. A., Murrough, J. W., & Abdallah, C. G. (2016) · Springer eBooks · doi:10.1007/978-3-319-42925-0_7 · Cited by 5
Estrogenic Regulation of Hippocampal Neurogenesis Throughout the Lifespan
Yagi, S., Eid, R. S., Qiu, W., Duarte‐Guterman, P., & Galea, L. A. M. (2020) · Oxford University Press eBooks · doi:10.1093/oso/9780190645908.003.0016 · Cited by 4
Adult Neural Stem Cells as Promising Targets in Psychiatric Disorders
Rodrigues, R. S., Paulo, S. L., Moreira, J. B., Tanqueiro, S. R., Sebastião, A. M., Diógenes, M. J., & Xapelli, S. (2020) · Stem Cells and Development · doi:10.1089/scd.2020.0100 · Cited by 4
“Similarly, other studies have shown that mood-improving actions promoted by antidepressants may depend on other brain mechanisms, like hippocampal and PFC neuronal remodeling, rather than AHN by itself [133,134].”
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StressMatic: A Novel Automated System to Induce Depressive- and Anxiety-like Phenotype in Rats
Martins‐Macedo, J., Mateus‐Pinheiro, A., Alves, C. S. C., Veloso, F., Gomes, E. D., Ribeiro, I., Correia, J. S., Silveira‐Rosa, T., Alves, N. D., Rodrigues, A. J., et al. (2023) · Cells · doi:10.3390/cells12030381 · Cited by 4
“The individual preference for sucrose was calculated using the following formula: sucrose preference = (sucrose intake)/(sucrose intake + water intake) × 100, as previously described [20].”
MethodSelf-citationEpigenetic regulation of BDNF-TrkB signaling in the pathophysiology and treatment of mood disorders
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Valencia-Flores, K., Yahel Vidal de la, O., Paz-Trejo, D. B., & Sánchez-Castillo, H. (2025) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2025.05.001 · Cited by 4
“Fluoxetine has been validated as a powerful treatment to reduce anxiety (Levone et al., 2021), depression (Bessa et al., 2009), and cognitive impairments in patients with MDD (Song, Che, Min-Wei, Murakami, & Matsumoto, 2006).”
A Review on Diagnostic Proteomics of Depression
Samad, N. (2017) · MOJ Proteomics & Bioinformatics · doi:10.15406/mojpb.2017.06.00187 · Cited by 2
Novel experimental and early investigational drugs for the treatment of bipolar disorder
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“plasma concentration of the progesterone derivative allopregnanolone is elevated in the premenstrual period of euthymic women with BD compared to healthy controls and women with major depressive disorder [50,51].”
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ROLE OF HIPPOCAMPAL NEUROGENESIS IN THE PATHOPHYSIOLOGY AND TREATMENT OF DEPRESSION
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Agomelatine – pharmacological properties and use in psychiatric practice
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“W licznych zwierzęcych modelach depresji obserwowano zmniejszenie objętości hipokampa, natomiast podawanie zwierzętom laboratoryjnym skutecznych LPD prowadziło do wzrostu objętości hipokampa poprzez wzrost proliferacji neuronów i zahamowanie apoptozy komórek (Bessa et al., 2009).”
BackgroundRapidly emerging adolescent nicotine-induced dendritic remodeling is D1-dopamine receptor dependent
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Neurogenic Basis of Antidepressant Action: Recent Advances
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Hormone Regulation of Neurogenesis Across the Lifespan
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Antidepressant-related microstructural changes in the external capsule
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“Evidence from animal models and in vivo studies indicates that antidepressant medications are strongly linked to brain microstructure alterations (Bessa et al., 2009).”
Characterization of Neurensin-2 knockout mice: insights into stress-resilience mechanisms
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Metadata
- Authors
- Bessa, J. M., Ferreira, D., Melo, I., Marques, F., Cerqueira, J. J., Palha, J. A., Almeida, O. F. X., & Sousa, N.
- Affiliations
- University of Minho (PT)
- Max Planck Society (DE)
- Corresponding author
- Sousa, N
- Venue
- Molecular Psychiatry
- Published
- 2008-11-04
- Volume
- 14
- Issue
- 8
- Pages
- 764-773
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W1983617759
- Cited by
- 598
- References
- 46
- Citations by year
- 2026: 9 · 2025: 17 · 2024: 11 · 2023: 33 · 2022: 30 · 2021: 38 · 2020: 26 · 2019: 33 · 2018: 31 · 2017: 48 · 2016: 37 · 2015: 44 · 2014: 53 · 2013: 38 · 2012: 48
- FWCI
- 23.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, cc-by-nc-nd)
- Funders
- Pfizer
- Sanofi
- Fundação para a Ciência e a Tecnologia (PTDC/SAU-NEU/72699/2006)
- National Cancer Institute (N02-CB-07008)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- antidepressants, neurogenesis, hippocampus, neuronal remodeling, dendritic remodeling, synaptic plasticity, depression, chronic mild stress, fluoxetine, imipramine, methylazoxymethanol, anhedonia, learned helplessness, prefrontal cortex, neuroplasticity
- MeSH terms
- Affect, Analysis of Variance, Animals, Antidepressive Agents, Behavior, Animal, Depression, Drug Combinations, Fluoxetine, Hippocampus, Imipramine, Indoles, Male, Methylazoxymethanol Acetate, Mitosis, Neuronal Plasticity, Pyrrolidines, Stress, Psychological, Rats, Wistar, Prefrontal Cortex, Receptors, Corticotropin-Releasing Hormone, Rats, Cytostatic Agents, Neurogenesis, Antidiuretic Hormone Receptor Antagonists
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