Control of Ciliary Beating of Schistosomal Miracidia

1998 Fiscal Year Final Research Report Summary

• Project/Area Number: 09670266
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: 寄生虫学(含医用動物学)
• Research Institution: NaGASAKI UNIVERSITY
• Principal Investigator: AOKI Yoshiki Institute of Tropical Medicine, NAGASAKI UNIVERSITY, Professor, 熱帯医学研究所, 教授 (90039925)
• Co-Investigator(Kenkyū-buntansha): KATSUMATA Tatsuya Institute of Tropical Medicine, NAGASAKI UNIVERSITY, Professor, 熱帯医学研究所, 助手 (10284712) ; NIWA Masami School of Medicine, NAGASAKI UNIVERSITY, Professor, 医学部, 教授 (20136641)
• Project Period (FY): 1997 – 1998
• Keywords: schistosome / miracidium / cilia / cAMP / potassium ion channel / protein k-inase A / chemotaxis / osmotic pressure

Research Abstract

Schistosomal miracidia are completely covered by numerous cilia. The vigorous beating of cilia of miracidia is the driving force of hatching of the egg, swimming in water and invasion into the intermediate snail. The present study aimed at examination of the control mechanism of ciliary beating of miracidia of Schistosoma manosni.
Although some external stimulus cause the change in the ciliary beating, the present study dealt with the control mechanism of ciliary beating by osmotic pressure and possible change of ciliaty beating in chemotactic swimming activity.
The highlights of the results are 1) that hatching of the eggs is caused by the combination of vigorous beating of cilia and swelling of eggshell, 2) that membrane permeable cAMP, forskokin and IBMX cause the ciliary beating of miracidia which remain to he quiet under high osmotic pressure. 3) that protein kinase A inhibitor and potassium ion channel blocker suppress the ciliary beating of miracidia which swim in water, 4) that membrane permeable cAMP, but not non-permeable cAMP, cause miracidia to take peculiar swimming activity which mimic the chemotactic (klinokinetic) activity of miracidia to snail conditioned water (SCW), and 5) that chemotactic activity of miracidia to SCW is inhibited by eserine.
Our results propose the possible control mechanism of ciliary beating of miracidia. Osmotic receptors are present over the integument of miracidia. When the receptors are activated by low osmotic pressure, potassium ion channel is activated. Influx of potassium ions activates adenyl cyclase. Then increase in cAMP concentration activates microtuble movement, then ciliary heating starts. When miracidia are exposed to high osmotic pressure, potassium ion channels are inactivated. Decrease in cAMP concentration suppress the ciliary beating. Chemotactic activity is not controlled by ciliary beating.