Cited by 667Treatment of Major DepressionNerve injury and regenerationNeurotransmitter Receptor Influence on Behavior

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Role of neurotrophic factors in depression

CASTREN, E, VOIKAR, V, RANTAMAKI, T·2007·Current Opinion in Pharmacology

DOI 10.1016/j.coph.2006.08.009

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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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RETRACTED: Electroconvulsive therapy and aerobic exercise training increased BDNF and ameliorated depressive symptoms in patients suffering from treatment-resistant major depressive disorder
Salehi, I., Hosseini, S. M., Haghighi, M., Jahangard, L., Bajoghli, H., Gerber, M., Pühse, U., Kirov, R., Holsboer‐Trachsler, E., & Brand, S. (2014) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2014.06.018 · Cited by 43
Retracted
Modulation of neuronal plasticity following chronic concomitant administration of the novel antipsychotic lurasidone with the mood stabilizer valproic acid
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Venlafaxine treatment stimulates expression of brain-derived neurotrophic factor protein in frontal cortex and inhibits long-term potentiation in hippocampus
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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)
DOI: 10.1016/j.coph.2006.08.009
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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

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