Role of neurotrophic factors in depression

    Research output: Contribution to journalReview ArticleScientificpeer-review

    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.
    Original languageEnglish
    JournalCurrent Opinion in Pharmacology
    Volume7
    Issue number1
    Pages (from-to)18-21
    Number of pages4
    DOIs
    Publication statusPublished - 2007
    MoE publication typeA2 Review article in a scientific journal

    Fields of Science

    • 311 Basic medicine
    • 118 Biological sciences
    • 515 Psychology

    Cite this

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    title = "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.",
    keywords = "311 Basic medicine, 118 Biological sciences, 515 Psychology",
    author = "Eero Castren and Vootele V{\~o}ikar and Tomi Rantam{\"a}ki",
    year = "2007",
    doi = "10.1016/j.coph.2006.08.009",
    language = "English",
    volume = "7",
    pages = "18--21",
    journal = "Current Opinion in Pharmacology",
    issn = "1471-4892",
    publisher = "Elsevier Scientific Publ. Co",
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    }

    Role of neurotrophic factors in depression. / Castren, Eero; Võikar, Vootele; Rantamäki, Tomi.

    In: Current Opinion in Pharmacology, Vol. 7, No. 1, 2007, p. 18-21.

    Research output: Contribution to journalReview ArticleScientificpeer-review

    TY - JOUR

    T1 - Role of neurotrophic factors in depression

    AU - Castren, Eero

    AU - Võikar, Vootele

    AU - Rantamäki, Tomi

    PY - 2007

    Y1 - 2007

    N2 - 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.

    AB - 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.

    KW - 311 Basic medicine

    KW - 118 Biological sciences

    KW - 515 Psychology

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    DO - 10.1016/j.coph.2006.08.009

    M3 - Review Article

    VL - 7

    SP - 18

    EP - 21

    JO - Current Opinion in Pharmacology

    JF - Current Opinion in Pharmacology

    SN - 1471-4892

    IS - 1

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