Cited by 193Treatment of Major DepressionNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

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Cellular and molecular mechanisms in the long-term action of antidepressants.

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Racagni, Giorgio, Popoli, Maurizio·2008·Dialogues in Clinical Neuroscience

DOI 10.31887/dcns.2008.10.4/gracagniPMC PMC3181899

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Abstract

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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Figure 1 Main classes of antidepressant drugs from the 1960s to present times. FGA, first-generation antidepressant; SGA, second-generation antidepressant; TGA, third-generation antidepressant (only the main classes of antidepressants in development are reported among TGAs, see also Table III). MAOI, monamine oxidase inhibitor; SSRI, selective serotonin reuptake inhibitor; SNRI, serotonin and noradrenaline reuptake inhibitor; NARI, noradrenaline reuptake inhibitor; SARI, serotonin 2, antagonist/ reuptake inhibitor; NASSA, noradrenergic and specific serotonergic antidepressant; MT, melatonin; 5-HT, serotonin; NK, neurokinin; CRF, corticotropin-releasing factor; Glu, glutamateCC BY-NC-ND · PubMed Central

Figure 2 Major signaling cascades involved in the activation of the transcription factor CREB and in the long-term action of antidepressants. A number of genes are depicted, whose transcription is regulated by CREB. Trk B, tyrosine kinase B; MARK, mitogen-activated protein kinase; RSK, ribosomal S6 kinase; CREB, cAMP response element binding protein; NMDA, N-methyl-D-aspartic acid; Glu, glutamate; PLC, phosphatase C; PDE, phosphodiesterase; AC, adenylate cyclase; cAMP; cyclic adenosine monophosphate; ATP, adenosine triphosphate; PKA, protein kinase A; TH, tyrosine hydroxylase; BDNF, brain-derived neurotrophic factor; AC -VIII, adenyl cyclase type VIII; CREm, CAMP-responsive element modulator; CRF, corticotropin-releasing factor, Syn, synaptopsin Reproduced from ref 3: Carlezon VVAJr, Duman RS, Nestler EJ. The many faces of CREB. Trends Neurosci. 2005;28:436-445. Copyright © Elsevier 2005CC BY-NC-ND · PubMed Central

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Seriesinfo
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Introduction
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The role of models in clinical reasoning
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Preface
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Epigraph
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How Psychiatrists Make Decisions
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Authors: Racagni, G., & Popoli, M.
Affiliations: University of Milan (IT)
Corresponding author: Popoli, Maurizio
ORCID: Racagni, Giorgio
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
DOI: 10.31887/dcns.2008.10.4/gracagni
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: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/3.0/ (vor)
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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Cellular and molecular mechanisms in the long-term action of antidepressants.

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