Thyroxin regulates BDNF expression to promote survival of injured neurons

    Research output: Contribution to journalArticleScientificpeer-review

    Abstract

    A growing amount of evidence indicates that neuronal trauma can induce a recapitulation of developmental-like mechanisms for neuronal survival and regeneration. Concurringly, ontogenic dependency of central neurons for brain-derived neurotrophic factor (BDNF) is lost during maturation but is re-acquired after injury. Here we show in organotypic hippocampal slices that thyroxin, the thyroid hormone essential for normal CNS development, induces up-regulation of BDNF upon injury. This change in the effect of thyroxin is crucial to promote survival and regeneration of damaged central neurons. In addition, the effect of thyroxin on the expression of the K-Cl cotransporter (KCC2), a marker of neuronal maturation, is changed from down to up-regulation. Notably, previous results in humans have shown that during the first few days after traumatic brain injury or spinal cord injury, thyroid hormone levels are often diminished. Our data suggest that maintaining normal levels of thyroxin during the early post-traumatic phase of CNS injury could have a therapeutically positive effect. (C) 2009 Elsevier Inc. All rights reserved.
    Original languageEnglish
    JournalMolecular and Cellular Neuroscience
    Volume42
    Issue number4
    Pages (from-to)408-418
    Number of pages11
    ISSN1044-7431
    DOIs
    Publication statusPublished - 2009
    MoE publication typeA1 Journal article-refereed

    Fields of Science

    • BDNF
    • Thyroxin
    • KCC2
    • Trophic support
    • Axotomy
    • Time-lapse microscopy
    • K+/CL-COTRANSPORTER KCC2
    • TRAUMATIC BRAIN-INJURY
    • DEVELOPMENTAL UP-REGULATION
    • SPINAL-CORD-INJURY
    • THYROID-HORMONE
    • MESSENGER-RNA
    • ADULT-RAT
    • NEUROTROPHIC FACTOR
    • NERVE REGENERATION
    • DOWN-REGULATION
    • 3112 Neurosciences

    Cite this

    @article{8430c4b7510048f68ac79b4f4e6a211c,
    title = "Thyroxin regulates BDNF expression to promote survival of injured neurons",
    abstract = "A growing amount of evidence indicates that neuronal trauma can induce a recapitulation of developmental-like mechanisms for neuronal survival and regeneration. Concurringly, ontogenic dependency of central neurons for brain-derived neurotrophic factor (BDNF) is lost during maturation but is re-acquired after injury. Here we show in organotypic hippocampal slices that thyroxin, the thyroid hormone essential for normal CNS development, induces up-regulation of BDNF upon injury. This change in the effect of thyroxin is crucial to promote survival and regeneration of damaged central neurons. In addition, the effect of thyroxin on the expression of the K-Cl cotransporter (KCC2), a marker of neuronal maturation, is changed from down to up-regulation. Notably, previous results in humans have shown that during the first few days after traumatic brain injury or spinal cord injury, thyroid hormone levels are often diminished. Our data suggest that maintaining normal levels of thyroxin during the early post-traumatic phase of CNS injury could have a therapeutically positive effect. (C) 2009 Elsevier Inc. All rights reserved.",
    keywords = "BDNF, Thyroxin, KCC2, Trophic support, Axotomy, Time-lapse microscopy, K+/CL-COTRANSPORTER KCC2, TRAUMATIC BRAIN-INJURY, DEVELOPMENTAL UP-REGULATION, SPINAL-CORD-INJURY, THYROID-HORMONE, MESSENGER-RNA, ADULT-RAT, NEUROTROPHIC FACTOR, NERVE REGENERATION, DOWN-REGULATION, 3112 Neurosciences",
    author = "Anastasia Shulga and Anne Blaesse and Kysenius, {Kai Johannes} and Huttunen, {Henri J.} and Kimmo Tanhuanp{\"a}{\"a} and Mart Saarma and Claudio Rivera",
    year = "2009",
    doi = "10.1016/j.mcn.2009.09.002",
    language = "English",
    volume = "42",
    pages = "408--418",
    journal = "Molecular and Cellular Neuroscience",
    issn = "1044-7431",
    publisher = "ACADEMIC PRESS INC ELSEVIER SCIENCE",
    number = "4",

    }

    Thyroxin regulates BDNF expression to promote survival of injured neurons. / Shulga, Anastasia; Blaesse, Anne; Kysenius, Kai Johannes; Huttunen, Henri J.; Tanhuanpää, Kimmo; Saarma, Mart; Rivera, Claudio.

    In: Molecular and Cellular Neuroscience, Vol. 42, No. 4, 2009, p. 408-418.

    Research output: Contribution to journalArticleScientificpeer-review

    TY - JOUR

    T1 - Thyroxin regulates BDNF expression to promote survival of injured neurons

    AU - Shulga, Anastasia

    AU - Blaesse, Anne

    AU - Kysenius, Kai Johannes

    AU - Huttunen, Henri J.

    AU - Tanhuanpää, Kimmo

    AU - Saarma, Mart

    AU - Rivera, Claudio

    PY - 2009

    Y1 - 2009

    N2 - A growing amount of evidence indicates that neuronal trauma can induce a recapitulation of developmental-like mechanisms for neuronal survival and regeneration. Concurringly, ontogenic dependency of central neurons for brain-derived neurotrophic factor (BDNF) is lost during maturation but is re-acquired after injury. Here we show in organotypic hippocampal slices that thyroxin, the thyroid hormone essential for normal CNS development, induces up-regulation of BDNF upon injury. This change in the effect of thyroxin is crucial to promote survival and regeneration of damaged central neurons. In addition, the effect of thyroxin on the expression of the K-Cl cotransporter (KCC2), a marker of neuronal maturation, is changed from down to up-regulation. Notably, previous results in humans have shown that during the first few days after traumatic brain injury or spinal cord injury, thyroid hormone levels are often diminished. Our data suggest that maintaining normal levels of thyroxin during the early post-traumatic phase of CNS injury could have a therapeutically positive effect. (C) 2009 Elsevier Inc. All rights reserved.

    AB - A growing amount of evidence indicates that neuronal trauma can induce a recapitulation of developmental-like mechanisms for neuronal survival and regeneration. Concurringly, ontogenic dependency of central neurons for brain-derived neurotrophic factor (BDNF) is lost during maturation but is re-acquired after injury. Here we show in organotypic hippocampal slices that thyroxin, the thyroid hormone essential for normal CNS development, induces up-regulation of BDNF upon injury. This change in the effect of thyroxin is crucial to promote survival and regeneration of damaged central neurons. In addition, the effect of thyroxin on the expression of the K-Cl cotransporter (KCC2), a marker of neuronal maturation, is changed from down to up-regulation. Notably, previous results in humans have shown that during the first few days after traumatic brain injury or spinal cord injury, thyroid hormone levels are often diminished. Our data suggest that maintaining normal levels of thyroxin during the early post-traumatic phase of CNS injury could have a therapeutically positive effect. (C) 2009 Elsevier Inc. All rights reserved.

    KW - BDNF

    KW - Thyroxin

    KW - KCC2

    KW - Trophic support

    KW - Axotomy

    KW - Time-lapse microscopy

    KW - K+/CL-COTRANSPORTER KCC2

    KW - TRAUMATIC BRAIN-INJURY

    KW - DEVELOPMENTAL UP-REGULATION

    KW - SPINAL-CORD-INJURY

    KW - THYROID-HORMONE

    KW - MESSENGER-RNA

    KW - ADULT-RAT

    KW - NEUROTROPHIC FACTOR

    KW - NERVE REGENERATION

    KW - DOWN-REGULATION

    KW - 3112 Neurosciences

    U2 - 10.1016/j.mcn.2009.09.002

    DO - 10.1016/j.mcn.2009.09.002

    M3 - Article

    VL - 42

    SP - 408

    EP - 418

    JO - Molecular and Cellular Neuroscience

    JF - Molecular and Cellular Neuroscience

    SN - 1044-7431

    IS - 4

    ER -