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Role of neurotrophic factors in depression
Abstract
Major depression is associated with reduced volumes in the hippocampus and prefrontal cortex, whereas antidepressant treatments promote several forms of neuronal plasticity, including neurogenesis, synaptogenesis and neuronal maturation, in the hippocampus. Several neurotrophic factors are associated with depression or antidepressant action. Stress suppresses brain-derived neurotrophic factor (BDNF) synthesis in the hippocampus, at least partially through a sustained modification of chromatin structure. Essentially all antidepressant treatments increase BDNF synthesis and signaling in the hippocampus and prefrontal cortex. This signaling is required for the behavioral effects of antidepressant drugs in rodents, and increased BDNF levels in the hippocampus mimic the behavioral effects of antidepressants. However, injection of BDNF into the mesolimbic dopamine pathway produces an opposing depression-like response. One hypothesis emerging from these data proposes that mood disorders reflect failed function of critical neuronal networks, whereas a gradual network recovery through activity-dependent neuronal plasticity induces the antidepressant effect. Neurotrophic factors themselves do not control mood, but they act as necessary tools in the activity-dependent modulation of networks, the physiological function of which determines how a plastic change influences mood.
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“These results lend substantial support to the neuroplasticity hypothesis of depression (sometimes referred to as the neurotrophin hypothesis) (11, 23–36).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [28]
In the citing paper
“A growing body of research suggests that neuroplasticity pathways play a significant role in the pathophysiology of depression and in the therapeutic mechanisms of antidepressant drugs (AD) [1,2,3].”
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Metadata
- Authors
- CASTREN, E., VOIKAR, V, & RANTAMAKI, T.
- Venue
- Current Opinion in Pharmacology
- Publisher
- Elsevier BV
- Published
- 2007-02
- Volume
- 7
- Issue
- 1
- Pages
- 18-21
- ISSN
- 1471-4892 (ISSN-L)
- OpenAlex
- W1993636230
- Cited by
- 667
- References
- 32
- Citations by year
- 2026: 8 · 2025: 18 · 2024: 17 · 2023: 20 · 2022: 13 · 2021: 24 · 2020: 30 · 2019: 23 · 2018: 31 · 2017: 32 · 2016: 33 · 2015: 57 · 2014: 38 · 2013: 40 · 2012: 59
- FWCI
- 25.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- neurotrophic factors, major depressive disorder, brain-derived neurotrophic factor, antidepressant mechanism, hippocampus, prefrontal cortex, neuroplasticity, neurogenesis, synaptogenesis, chronic stress, chromatin structure, mesolimbic dopamine system, activity-dependent plasticity, mood disorders
- MeSH terms
- Animals, Antidepressive Agents, Depression, Humans, Nerve Growth Factors, Stress, Physiological, Mood Disorders
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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