CILIARY BEATING OF SCHISTOSOMA MIRACIDIUM-POSSIBLE INVOLVEMENT OF CYCLIC NCLEOTIDE AND ION CHANNEL

蟋蟀血吸虫纤毛跳动-可能涉及环核苷酸和离子通道

• 批准号: 07670285
• 负责人: AOKI Yoshiki
• 金额: $ 1.54万
• 依托单位: NAGASAKI UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07670285/
• 关键词: schistosome; miracidia; cilia; cAMP; cGMP; protein kinase A; K^+channel; イオンチャネル

The studies on regulation of ciliary motility in Paramecium encouraged us to investigate the control mechanisms of ciliary beat of schistosome miracidia. The present study aimed at investigating the possible involvement of cAMP,cGMP,protein kinase A and ion channels in signal transduction mechanisms of ciliary beat of schistosome miracidia.Schistosome miracidia swim in water by means of numerous cilia which cover the body surface. The miracidia stop swimming in 1% NaCL solution. Addition of membrane permeable cAMP or cGMP causes about 40% of miracidia to swim under high osmotic pressure, the swimming speed is about 1/6 of that of miracidia swimming in water though. Addition of forskolin, an activator of adenyl cyclase and guanyl cyclase, and IBMX,an inhibitor or phosphodiesterase also caused miracidial forward swimming. The effect of these reagents was dose dependent.Cholera toxin increases adenyl cyclase activity of metazoan via tis effect on G-protein. However, cholera toxin did not have any effect on ciliary beat of miracidia. Inhibitor of protein kinase A,H88 and H89, inhibited miracidial swimming in water. K^+channel blocker, quinine and alpha dendrotixin, caused swimming of miracidia in water. Inhibitory effect of H88, H89, quinine and alpha dendrotoxin was dose dependent. Na^+channel blocker and Ca^<++>channel blocker did not have any effect on swimming of miracidia.These results suggest that cyclic nucleotide, protein kinase A and K^+channel regulate ciliary beat of schistosome miracidia.

对甲虫中睫状运动调节的研究鼓励我们研究奇迹般的奇迹般的纤毛拍打的控制机制。本研究旨在研究CAMP，CGMP，CGMP，蛋白激酶A和离子通道可能参与，这是黑素奇迹般的纤毛粉刺的信号转导机制。通过覆盖身体表面的许多cilia，在水中游泳奇迹般的奇迹。奇迹停止在1％NaCl溶液中游泳。增加膜渗透的营地或CGMP会导致大约40％的奇迹在高渗透压下游泳，但游泳速度约为Miracidia在水中游泳的1/6。添加了腺基环酶和鸟烯基环基酶的激活剂，以及抑制剂或磷酸二酯酶的IBMX激活剂也引起了奇迹前进的游泳。这些试剂的作用是剂量依赖性。胆碱毒素通过TIS对G蛋白的作用增加了后生动物的腺基环化酶活性。但是，霍乱毒素对奇迹般的睫毛粉没有任何影响。蛋白激酶A，H88和H89的抑制剂抑制了水中的奇迹游泳。 K^+通道阻滞剂，奎宁和α树突蛋白在水中引起奇迹游泳。 H88，H89，奎宁和α树突毒素的抑制作用均取决于剂量。 Na^+通道阻滞剂和Ca^<++>通道阻滞剂对奇迹的游泳没有任何影响。这些结果表明，环状核苷酸，蛋白激酶A和K^+通道调节了奇迹般的奇迹般的纤毛粉刺。