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First published online June 29, 2006
Journal of Experimental Biology 209, 2765-2773 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02377

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Nervous control of ciliary beating by Cl^-, Ca²⁺ and calmodulin in Tritonia diomedea

Owen M. Woodward^1,2,* and A. O. Dennis Willows^1,2

¹ Department of Biology, University of Washington, Box 351800, Seattle, WA 98195, USA
² Friday Harbor Laboratories, University of Washington, 620 University Road, Friday Harbor, WA 98250, USA

^* Author for correspondence at present address: Department of Physiology, Johns Hopkins School of Medicine, 725 N. Wolfe Street, 214 WBSB, Baltimore, MD 21205, USA (e-mail: owenw{at}jhmi.edu)

Accepted 8 June 2006

In vertebrates, motile cilia line airways, oviducts and ventricles. Invertebrate cilia often control feeding, swimming and crawling, or gliding. Yet control and coordination of ciliary beating remains poorly understood. Evidence from the nudibranch mollusc, Tritonia diomedea, suggests that locomotory ciliated epithelial cells may be under direct electrical control. Here we report that depolarization of ciliated pedal epithelial (CPE) cells increases ciliary beating frequency (CBF), and elicits CBF increases similar to those caused by dopamine and the neuropeptide, TPep-NLS. Further, four CBF stimulants (zero external Cl^-, depolarization, dopamine and TPep-NLS) depend on a common mode of action, viz. Ca²⁺ influx, possibly through voltage-gated Ca²⁺ channels, and can be blocked by nifedipine. Ca²⁺ influx alone, however, does not provide all the internal Ca²⁺ necessary for CBF change. Ryanodine receptor (RyR) channel-gated internal stores are also necessary for CBF excitation. Caffeine can stimulate CBF and is sensitive to the presence of the RyR blocker dantrolene. Dantrolene also reduces CBF excitation induced by dopamine and TPep-NLS. Finally, W-7 and calmidazolium both block CBF excitation by caffeine and dopamine, and W-7 is effective at blocking TPep-NLS excitation. The effects of calmidazolium and W-7 suggest a role for Ca²⁺-calmodulin in regulating CBF, either directly or via Ca²⁺-calmodulin dependent kinases or phosphodiesterases. From these results we hypothesize dopamine and TPep-NLS induce depolarization-driven Ca²⁺ influx and Ca²⁺ release from internal stores that activates Ca²⁺-calmodulin, thereby increasing CBF.

Key words: Tritonia diomedea, ciliary beat frequency, dopamine, TPep, intracellular Ca²⁺, Cl^-, calmodulin, ryanodine receptor