The DOI matches its Crossref record; 125 of the 125 references it cites were found in a registry or an index.
Cellular and molecular mechanisms in the long-term action of antidepressants.
Open accessAbstract
The hypotheses on the pathophysiology of depression/mood disorders and on antidepressant mechanisms have greatly changed in recent years. The classical monoamine hypothesis was revealed to be simplistic, in that it could not explain the temporal delay in the therapeutic action of antidepressants. Converging lines of evidence have shown that adaptive changes in the several mechanisms of neuroplasticity are likely to be the cellular and molecular correlates of therapeutic effect. In this article, several mechanisms of neuroplasticity are analyzed in relation to the mechanism of antidepressants, ranging from changes in gene expression (including neurotrophic mechanisms), to synaptic transmission and plasticity, and neurogenesis. We propose that the current version of the hypothesis of antidepressant mechanism simply be called the "hypothesis of neuroplasticity". In the final section, we also briefly review the main current novel strategies in the pharmacology of depression and the new putative targets for antidepressants, with particular emphasis on nonmonoaminergic mechanisms.
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“Tricyclics, MAO inhibitors, and SSRIs all increase synaptic levels of monoamines in the brain within minutes, while it takes weeks before the antidepressant effects become apparent (Figure 1) (4, 9).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [4]
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“the primary issue with the monoamine hypothesis of depression lies in the temporal discrepancy between the acute effects of traditional antidepressants and their delayed therapeutic responses”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [4]
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Cites
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Cited by
Sorted by citations
Towards a glutamate hypothesis of depression
Sanacora, G., Treccani, G., & Popoli, M. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2011.07.036 · Cited by 1,036
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From Serotonin to Neuroplasticity: Evolvement of Theories for Major Depressive Disorder
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Metadata
- Authors
- Racagni, G., & Popoli, M.
- Affiliations
- University of Milan (IT)
- Corresponding author
- Popoli, Maurizio
- Venue
- Dialogues in Clinical Neuroscience
- Publisher
- Informa UK Limited
- Published
- 2008-12-31
- Volume
- 10
- Issue
- 4
- Pages
- 385-400
- ISSN
- 1294-8322 (ISSN-L)
- 1958-5969
- PMC
- PMC3181899
- OpenAlex
- W2095618681
- Cited by
- 192
- References
- 125
- Citations by year
- 2026: 6 · 2025: 26 · 2024: 12 · 2023: 5 · 2022: 14 · 2021: 13 · 2020: 7 · 2019: 7 · 2018: 5 · 2017: 10 · 2016: 13 · 2015: 8 · 2014: 16 · 2013: 10 · 2012: 10
- FWCI
- 7.03
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- Locations
- Dialogues in Clinical Neuroscience (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- antidepressants, depression, mood disorders, neuroplasticity, antidepressant mechanism, monoamine hypothesis, gene expression, neurotrophic factors, synaptic plasticity, synaptic transmission, neurogenesis
- MeSH terms
- Animals, Antidepressive Agents, Depressive Disorder, Humans, Synaptic Transmission, Neuronal Plasticity, Neurons, Biogenic Monoamines, Brain-Derived Neurotrophic Factor, Cell Proliferation
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