Glial Reaction in the Spinal Cord of the Degenerating Muscle Mouse (Scn8a dmu )
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  • 作者:Tadasu Sato (1)
    Masatoshi Fujita (1)
    Yoshinaka Shimizu (1)
    Hiroyasu Kanetaka (2)
    Leona W. G. Chu (3)
    Patrice D. C么t茅 (3)
    Hiroyuki Ichikawa (1)

    1. Division of Oral and Craniofacial Anatomy
    ; Tohoku University Graduate School of Dentistry ; Sendai ; 980-8575 ; Japan
    2. Graduate School of Biomedical Engineering
    ; Tohoku University ; Sendai ; 980-8577 ; Japan
    3. Department of Biology
    ; Dalhousie University ; Halifax ; NS ; B3H 4R2 ; Canada
  • 关键词:Degenerating muscle mouse ; Astrocyte ; Microglia ; Spinal cord ; Motor neuron ; Immunohistochemistry
  • 刊名:Neurochemical Research
  • 出版年:2015
  • 出版时间:January 2015
  • 年:2015
  • 卷:40
  • 期:1
  • 页码:124-129
  • 全文大小:3,849 KB
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    4. Sato T, Shimizu Y, Kano M, Suzuki T, Kanetaka H, Chu LW, C么t茅 PD, Shimauchi H, Ichikawa H (2011) Increase of CGRP expression in motor endplates within fore and hind limb muscles of the degenerating muscle mouse ( / Scn8a / dmu ). Cell Mol Neurobiol 31:155鈥?61 CrossRef
    5. Ichikawa H, Kano M, Shimizu Y, Suzuki T, Sawada E, Ono W, Chu LW, C么t茅 PD (2010) Increase of c-Fos and c-Jun expression in spinal and cranial motoneurons of the degenerating muscle mouse ( / Scn8a / dmu ). Cell Mol Neurobiol 30:737鈥?42 CrossRef
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  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Biomedicine
    Neurosciences
    Biochemistry
    Neurology
  • 出版者:Springer Netherlands
  • ISSN:1573-6903
文摘
The glial reaction was investigated in the spinal cord of the degenerating muscle (dmu) mouse, which harbours a null mutation in the voltage-gated sodium channel gene Scn8a and does not produce functional Nav1.6 channel. Glial fibrillary acidic protein (GFAP)- and Iba1-immunoreactivity were detected in numerous cells throughout the spinal cord of wild type mice. These cells had small cell bodies and ramified processes. The dmu mutation increased the number of GFAP-immunoreactive (-IR) cells and the length of their processes in the ventral horn but not in the dorsal horn of the lumbar spinal cord. The number of Iba1-IR cells was similar in cervical and lumbar spinal cords of wild type and dmu mice. However, Iba1-IR processes and their branches became thinner and showed a fine varinose appearance in dmu mice. The length of Iba1-IR processes was significantly reduced in dorsal and ventral horns of dmu mice. Double immunofluorescence also demonstrated the relationship between glial cells and motor neurons containing calcitonin gene-related peptide (CGRP), a marker for their degeneration. The dmu mutation caused increase in the length of GFAP-IR processes surrounding CGRP-IR motor neurons in the ventral horn. However, the thickness and length of Iba1-IR processes around CGRP-IR motor neurons were reduced by the mutation. The present study suggests that the dmu mutation causes astrocytic activation and microglial inactivation in the spinal cord. These changes may be associated with degeneration and activity of motor and sensory neuron in dmu mice.

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