| Project/Area Number |
63304032
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Yokohama City University |
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Principal Investigator |
TAKENAKA Toshifumi Yokohama, City Univ. Physiology, Prof.,, 医学部, 教授 (00045999)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Junichiro Kyushu Dental Univ. Physiology, Prof., 歯学部, 教授 (60076015)
CHIHARA Etsuo Kyoto Univ,. Ophtalmology, Lecture., 医学部, 講師 (20111958)
FUJISAWA Koushiro Tokyo Metropolian Instit. for Neurosci., Chairman., 神経病理学研究室, 参事研究員 (90073064)
KOMIYA Yoshiaki Gunma Univ., Biochem., Prof., 医学部, 教授 (50010046)
HIROKAWA Nobutaka Tokyo Univ., Anatomy, Prof.., 医学部, 教授 (20010085)
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| Project Period (FY) |
1988 – 1990
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| Keywords | axoplasmic transport / kinesin / tissue cultured cell / neuronal dystrophy / microtubule / cytoskelet / neurotransmitter / MAPS |
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| Research Abstract |
The molecular physiological study of axoplasmic transport has been done in the three fields, cell cytoskeletal, physicobiochemical, and clinical medicine. Kinesin was found on the membrane organella moving anterogradely and dynein was found on the membrane organella moving both anterogradely and retrogradely. Microtubule was divided into three types, depolymerized, dynamic and stable types. These three types changes each other depending on physiological and pathological condition. These experiments were done 35 S-methionin labeling. The axoplasmic transport of mitochondria was studied by the video-enhanced microscope. The number of mitochondria passing though axon was twice in retrograde direction than in anterograde direction. The size of mitochondria moving retrogradely was about half compared with that of mitochondria moving anterogradely. These data implies that mitochondria divided into two in the terminal portion of axon. The latex beads coated with fluorescent dye was introduced into the cell body by the cell fusion method. This latex beads moving in the axon as the same movements of cell organella. The effect of neurotransmitter or the axoplasmic transport was also examined. Acetylcholin stopped the axoplasmic transport reversibly in the superior cervical ganglion. Muscarine receptor related in this effect. Glaucoma axonal dystrophy was also studied pathologically and was found that the anomaly of protein digestive enzyme was the main reason of this dystrophy. The recovery process of axoplasmic transport was also studied after transplantation. Glaucoma was also studied and its pathogenesis was related with the disorder of the axoplasmic transport.
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