دورية أكاديمية
Nervous control of ciliary beating by Cl(-), Ca(2+) and calmodulin in Tritonia diomedea.
| العنوان: | Nervous control of ciliary beating by Cl(-), Ca(2+) and calmodulin in Tritonia diomedea. |
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| المؤلفون: | Woodward OM; Department of Biology, University of Washington, Box 351800, Seattle, WA 98195, USA. owenw@jhmi.edu, Willows AO |
| المصدر: | The Journal of experimental biology [J Exp Biol] 2006 Jul; Vol. 209 (Pt 14), pp. 2765-73. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: Company Of Biologists Limited Country of Publication: England NLM ID: 0243705 Publication Model: Print Cited Medium: Print ISSN: 0022-0949 (Print) Linking ISSN: 00220949 NLM ISO Abbreviation: J Exp Biol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: London : Company Of Biologists Limited Original Publication: London, Cambridge Univ. Press. |
| مواضيع طبية MeSH: | Calcium/*metabolism , Calmodulin/*metabolism , Chlorides/*metabolism , Cilia/*physiology , Tritonia Sea Slug/*physiology, Caffeine/pharmacology ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Cilia/drug effects ; Neuropeptides ; Nifedipine/pharmacology ; Ryanodine Receptor Calcium Release Channel/metabolism ; Tritonia Sea Slug/cytology ; Tritonia Sea Slug/drug effects |
| مستخلص: | 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. Ca(2+) influx, possibly through voltage-gated Ca(2+) channels, and can be blocked by nifedipine. Ca(2+) influx alone, however, does not provide all the internal Ca(2+) 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 Ca(2+)-calmodulin in regulating CBF, either directly or via Ca(2+)-calmodulin dependent kinases or phosphodiesterases. From these results we hypothesize dopamine and TPep-NLS induce depolarization-driven Ca(2+) influx and Ca(2+) release from internal stores that activates Ca(2+)-calmodulin, thereby increasing CBF. |
| معلومات مُعتمدة: | F31 NS047922 United States NS NINDS NIH HHS; 5 F31 NS047922-02 United States NS NINDS NIH HHS |
| المشرفين على المادة: | 0 (Calmodulin) 0 (Chlorides) 0 (Neuropeptides) 0 (Ryanodine Receptor Calcium Release Channel) 3G6A5W338E (Caffeine) I9ZF7L6G2L (Nifedipine) SY7Q814VUP (Calcium) |
| تواريخ الأحداث: | Date Created: 20060701 Date Completed: 20060913 Latest Revision: 20200305 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1242/jeb.02377 |
| PMID: | 16809467 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 0022-0949 |
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| DOI: | 10.1242/jeb.02377 |