Developmental Delay in Islet-1-Positive Motor Neurons in Chick Spina Bifida

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  • WANG Min
    Department of Anatomy and Embryology, Ehime University Graduate School of Medicine Central Laboratory, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University
  • MOMINOKI Katsumi
    Department of Biological Resources, Integrated Center for Science, Ehime University Department of Animal Resources, Advanced Science Research Center, Okayama University
  • KINUTANI Masae
    Department of Basic Health Science, School of Nursing, Ehime University
  • WANG Zhong
    Department of Anatomy and Embryology, Ehime University Graduate School of Medicine Central Laboratory, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University
  • KOBAYASHI Naoto
    Medical Education, Ehime University Graduate School of Medicine
  • SHIMOKAWA Tetsuya
    Department of Anatomy and Embryology, Ehime University Graduate School of Medicine
  • NABEKA Hiroaki
    Department of Anatomy and Embryology, Ehime University Graduate School of Medicine
  • FUJIWARA Takashi
    Central Laboratory, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University
  • MATSUDA Seiji
    Department of Anatomy and Embryology, Ehime University Graduate School of Medicine

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Other Title
  • Anatomy: Developmental delay in Islet-1-positive motor neurons in chick spina bifida
  • Chronological changes in Islet-1-positive neurons in a chick model of spina bifida aperta

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Abstract

Spina bifida aperta (SBA) is a congenital malformation of the spinal cord with complications such as spinal ataxia and bowel and bladder dysfunction. We have developed a chick model with surgery-induced SBA that shows spinal ataxia after hatching. In the present study, motor neurons in the early stages in chicks with and without SBA were observed by immunohistochemical staining with a monoclonal antibody against Islet-1, a motor neuron marker. Delay in migration and maturation of motor neurons was observed in SBA. Although the final numbers of Islet-1-positive neurons in these two groups were not different, a defect in the production and elimination of excess motor neurons in the early developmental stages in the SBA group may be involved in the pathological mechanism of the motor complications of this disease.<br>

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