Physiology and Pathophysiology of Axonal Transport
Physiology and Pathophysiology of Axonal Transport
批准号:
06304054
负责人:
KOMIYA Yoshiaki
金额:
$5.31万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Co-operative Research (A)
财政年份:
1994
资助国家:
日本
项目状态:
已结题
起止时间:
1994 至 1995
中文摘要
对大约10个激动素家族成员进行了分子表征,证实轴突细胞骨架不是以聚合态(Hirokawa)转运的。在培养的交感神经元(Takenaka)中,快速轴突运输被乙酰胆碱抑制,而被肾上腺素增强。在大鼠(Amano)中,向张口肌发送轴突的神经元与向闭合肌肉发送轴突的神经元中,乙酰胆碱酯酶的活性不同。老年猴薄束核轴突营养不良在形态上不同于大鼠(Fuzisawa)。分析了海绵体神经元的轴突结构与轴突运输的关系(Koike)。在培养的神经元中,光照射轴突延长端(GOTO)可抑制轴突的快速运输,而轴突微管与轴突成熟(Komiya)有关。在几种运动神经元病(Toyota Oshima)中发现快速轴突运输受损,在几种神经系统疾病(Oka)的人腓肠神经活检标本中微管稳定性降低,移植神经出现少量的形态变化,提示快速轴突运输(Kohshima)的改变。IDPN(Komiya)给药后不久,神经细丝蛋白的磷酸化水平降低,β-溴苯基乙酰尿素处理的大鼠(Oka)的逆行轴突运输减少,实验性糖尿病大鼠的快速轴突运输受损,尤其是在低氧应激(Nagata)下。
英文摘要
About 10 members of kinesin family were characterized molecularly, and it was confirmed that axonal cytoskeleton was not transported in the polymerized form (Hirokawa). Fast axonal transport was inhibited by acetylcholine and augumented by adrenaline in the sympathetic neurons in culture (Takenaka). The activity of acetylcholinesterase was found to be different in the neurons sending their axons to mouth-opening muscle from those to closing one in the rat (Amano). Axonal dystrophy in the old monkey gracile nuclei was different morphologically from those in the rat (Fuzisawa). Axonal structure was analyzed in the Aplysial neurons in relation to axonal transport (Koike). In cultured neurons, fast axonal transport was inhibited by light irradiation to the elongating tip of neurite (Goto), and axonal microtubule were stabilized in relation to axonal maturation (Komiya). Fast axonal transport was suggested to be impaired in several motor neuron diseases (Toyoshima), microtubular stability was decreased in biopsy specimens of human sural nerve with several neurological disorders (Oka), and a few morphologacal changes were shown in the transplanted nerves, suggesting the changes of fast axonal transport (Kohshima). Phosphorylation of neurofilament proteins was found decreased in the initial phase soon after administration of IDPN (Komiya), retrograde axonal tranaport was suggested to be decreased in the beta-bromophenylacetylurea treated rat (Oka), and fast axonal transport was impaired in the experimental diabetic rat especially when exposed to hypoxic stress (Nagata).
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通讯作者:
Kano, M., Tashiro, H., Kawakami, T., Takenaka, T.& Gotoh, H.: "Light irradiation effect on axoplasmic transport in mammalian neurons." Riken Review. 11. 59-60 (1995)
卡诺,M.,田代,H.,川上,T.,竹中,T.
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小池宏之、今西美智子: "立体構築法(連続切片標本の作成とコンピューター構築)" 細胞. 28. 110-115 (1996)
Hiroyuki Koike、Michiko Imanishi:“三维构造方法(连续切片标本的制备和计算机构造)”Cell。28. 110-115(1996)
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共 27 条
Dynamic Analysis of Axonal Cytoskeletons by Most Advanced Visualization Technique.
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批准号:11480229
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项目类别:Grant-in-Aid for Scientific Research (B).
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资助金额:$9.98万
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财政年份:1999
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负责人:KOMIYA Yoshiaki
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依托单位:
Regulation of Cytoskeletal Protein Dynamics in the Axon and Its Changes with Growth, Aging and Regeneration
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批准号:09480218
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$7.87万
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财政年份:1997
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负责人:KOMIYA Yoshiaki
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依托单位:
Molecular mechanism of the initial process of neuronal aging.-perturbation in transport and polymerization-depolymerization dynamics of axonal cytoskeleton.
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批准号:07458204
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$4.8万
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财政年份:1995
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负责人:KOMIYA Yoshiaki
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依托单位:
Axonal and nueronal degeneration in relation to balance changes in synthesis, transport and degradation of cytoskeletal proteins.
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批准号:01480152
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$4.42万
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财政年份:1989
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负责人:KOMIYA Yoshiaki
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依托单位:
Biochemical studies on the pathogenetic mechanism of toxic neuropathies by using axonal transport.
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批准号:61570136
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.47万
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财政年份:1986
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负责人:KOMIYA Yoshiaki
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依托单位:
国内基金
海外基金
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