Direct Monitoring of Intracellular Calcium Ions in Sea Anemone Tentacles Suggests Regulation of Nematocyst Discharge by Remote, Rare Epidermal Cells.

In tentacles of sea anemones, cnidocytes and adjacent supporting cells are believed to be independent receptor-effector complexes that regulate nematocyst discharge in response to exogenous N-acetylated sugars. When sugar chemoreceptors on supporting cells are activated, nematocyst discharge is two- to threefold greater than discharge without chemosensitization. To examine the role of Ca2+ as a second messenger in chemodetection of sugars, we used fluo-3 to monitor Ca2+ levels in epidermal cells of intact anemone tentacles. Certain epidermal cells exhibit relatively high Ca2+ both with and without chemosensitization. With chemosensitization, a two-to threefold increase occurs in the abundance of relatively rare cells exhibiting the highest Ca2+ levels. Timecourses depicting abundances of these rare cells in chemosensitized specimens show positive correlations to timecourses for nematocyst discharge from chemosensitized specimens and for labeling of chemoreceptors. Cnidocyte/supporting-cell complexes discharging nematocysts are about three times more abundant than the rare cells exhibiting the highest intracellular Ca2+ levels. One interpretation of these data is that the Ca2+-dependent regulation of nematocyst discharge occurring with chemosensitization involves intense Ca2+ signaling by remote, rare cells. This interpretation is inconsistent with the current model that portrays cnidocyte/supporting-cell complexes as independent effectors of nematocyst discharge.