Abstract
The phylum Cnidarians are aquatic animals, including jellyfish, hydra, sea anemones, and corals. They are the simplest metazoans having a nervous system and are diploblastic. Cnidarians are obligate predators that capture prey using specialized stinging cells called cnidocytes. The cnidocyte contains a nematocyst, which is a capsule containing an inverted, hollow tubule. Prey contacting the tentacle triggers the nematocyst tubule to rapidly evert; a process called discharge. The everting tubule penetrates and envenomates the prey, which is carried to the mouth by tentacle movements.
Generally both chemical and mechanical stimuli are needed to trigger discharge. The cnidocytes, in sea anemones, are surrounded by two or more supporting cells that have chemoreceptors and possibly contact-sensitive mechanoreceptors (CSMs). Therefore, the cnidocyte/supporting cell complex (CSCC) controls nematocyst discharge.
This project explores the chemoreceptor signaling pathway controlling nematocyst discharge from tentacles of the sea anemone, Aiptasia pallida. Chemoreceptors respond to N-acetylated sugars, such as N-acetylneuraminic acid (NANA), which occur on prey surfaces. When stimulated, this chemosensory pathway sensitizes CSMs to trigger nematocyst discharge in response to physical contact.
Indirect evidence suggested that the NANA chemosensory pathway acts through the intracellular second-messenger, cyclic-AMP (cAMP). We now show that NANA dose-dependently increases in situ cAMP levels in the ectodermal layer of tentacles from A. pallida, but has no effect on the endodermal cAMP content. In addition, NANA activates cAMP-dependent protein kinase (PKA) in whole tentacle homogenates.
High levels of extracellular Mg2+ are commonly used to anesthetize excised tentacles and to block discharge. We find that high levels of Mg2+ block the NANAstimulated cAMP increase. This supports the fact that high Mg2+ levels inhibit nematocyst discharge, but calls into question published findings in which NANAinduced changes in stereociliary bundle length of excised, Mg2+ -anesthetized tentacles are attributed to cAMP.
We also find that NANA stimulates calcium influx into isolated tentacle ectodermal cells and that the influx is sensitive to various L-type calcium channel blockers, including dihydropyridines. The coincidence of the desensitization region of the nematocyst discharge curve with those NANA concentrations that most stimulate calcium influx, suggests a role of NANA-stimulated calcium influx in desensitization.
LLU Discipline
Physiology
Department
Physiology
School
Graduate School
First Advisor
David A. Hessinger
Second Advisor
John Buchholz
Third Advisor
William H. Fletcher
Fourth Advisor
Glyne U. Thorington
Fifth Advisor
Lubo Zhang
Degree Name
Doctor of Philosophy (PhD)
Degree Level
Ph.D.
Year Degree Awarded
2000
Date (Title Page)
12-2000
Language
English
Library of Congress/MESH Subject Headings
Sea anemones -- physiology; Nematocysts; Spatial behavior -- physiology; Stress -- metabolism; Predatory Behavior; Calcium Channel Blockers -- pharmacology
Type
Dissertation
Page Count
xii; 89
Digital Format
Digital Publisher
Loma Linda University Libraries
Copyright
Author
Usage Rights
This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.
Recommended Citation
Ozacmak, Veysel Haktan, "The Roles of Ca2+ and cAMP in the Nematocyst Discharge of the Sea Anemone Tentacle" (2000). Loma Linda University Electronic Theses, Dissertations & Projects. 691.
https://scholarsrepository.llu.edu/etd/691
Collection
Loma Linda University Electronic Theses and Dissertations
Collection Website
http://scholarsrepository.llu.edu/etd/
Repository
Loma Linda University. Del E. Webb Memorial Library. University Archives