Neurobiological and clinical effects of the antidepressant tianeptine
Abstract
The precise neurobiological processes involved in depression are not clear, but it is recognized that numerous factors are involved, including changes in neurotransmitter systems and brain plasticity. Neuroplasticity refers to the ability of the brain to adapt functionally and structurally to stimuli. Impairment of neuroplasticity in the hippocampus, amygdala and cortex is hypothesized to be the mechanism by which cognitive function, learning, memory and emotions are altered in depression. The mechanisms underlying alterations in neuroplasticity are believed to relate to changes in neurotransmitters, hormones and growth factors. Structural changes in the hippocampus that have been proposed to be associated with depression include dendritic atrophy, reduced levels of cerebral metabolites, decreased adult neurogenesis (generation of new nerve cells) and reduced volume. Increased dendritic branching occurs in the basolateral nucleus of the amygdala. Reduced neuronal size and glial cell density occur in the prefrontal cortex. Clinically, tianeptine is an antidepressant effective in reducing symptoms of depression in mild to moderate-to-severe major depression, including over the long term. Tianeptine is also effective in alleviating the symptoms of depression-associated anxiety. It is generally well tolerated, with little sedation or cognitive impairment. The efficacy profile of tianeptine could be explained by its neurobiological properties observed in animal models. Tianeptine…
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The contribution of neurogenesis in the hippocampus to the etiology of depression and antidepressive treatment has been intensively investigated but is not definitely clear.
“The contribution of neurogenesis in the hippocampus to etiology of depression and antidepressive treatment has been intensively investigated but is not definitely clear (Kasper and McEwen, 2008;Malberg et al., 2000;Sahay and Hen, 2007;Santarelli et al., 2003).”
From Serotonin and neuroplasticity – Links between molecular, functional and structural pathophysiology in depression (2017) · cites this paper as Kasper and McEwen, 2008
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References 82 · Cited by 302
- Authors
- Kasper, S., & McEwen, B. S.
- Affiliations
- Medical University of Vienna (AT)
- Rockefeller University (US)
- Corresponding author
- Kasper, Siegfried
- Venue
- CNS Drugs
- Published
- 2008
- Volume
- 22
- Issue
- 1
- Pages
- 15-26
- ISSN
- 1172-7047 (ISSN-L)
- OpenAlex
- W2015063347
- Cited by
- 302
- References
- 82
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 10 · 2023: 4 · 2022: 5 · 2021: 9 · 2020: 160 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 6 · 2014: 11 · 2013: 16 · 2012: 15
- FWCI
- 8.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- CNS Drugs (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › 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
- tianeptine, antidepressants, depression, neuroplasticity, hippocampus, amygdala, prefrontal cortex, dendritic atrophy, adult neurogenesis, stress, glutamatergic neurotransmission, apoptosis, anxiolytic effects, cognitive function
- MeSH terms
- Animals, Antidepressive Agents, Tricyclic, Anxiety, Brain, Cognition, Depression, Humans, Memory, Synapses, Thiazepines, Glutamic Acid
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