Activated L-Type Calcium Channels Inhibit Chemosensitized Nematocyst Discharge from Sea Anemone Tentacles.

Because nematocyst discharge requires extracellular Ca, Ca channels have been suspected to be involved; but their identity and role have not been revealed. The majority of nematocysts that discharge from sea anemone tentacles are under the control of sensitizing chemoreceptors for -acetylated sugars (, -acetylneuraminic acid). Activated chemoreceptors predispose contact-sensitive mechanoreceptors to trigger discharge. We show that activating L-type Ca channels inhibits -acetylneuraminic acid-sensitized discharge, contrary to a previous suggestion. In addition, inhibiting L-type channels increases sensitivity to -acetylneuraminic acid. Specifically, we show that the L-type Ca channel activator (-)-Bay K 8644 dose-dependently inhibits -acetylneuraminic acid-sensitized discharge, as does raising ambient Ca levels. We also show that lowering extracellular Ca levels or adding any of several selective and chemically distinct L-type Ca channel blockers, including dihydropyridines, dose-dependently increases -acetylneuraminic acid sensitivity and broadens the dynamic range of -acetylneuraminic acid sensitization. Consistent with these functional findings, expresses an L-type Ca channel α subunit transcript that encodes a conserved dihydropyridine-binding site. Phylogenetic analysis confirms a close relationship of the Ca channel α subunit sequence between anemones, anthozoans, and cnidarians that extends into protostomal and deuterostomal bilaterians. We conclude that L-type Ca channel activity modulates -acetylneuraminic acid-sensitized nematocyst discharge in a push-pull manner depending on channel activity state. Our findings suggest that L-type channel activation promotes chemosensory desensitization, and we predict that -acetylneuraminic acid chemoreceptor signaling will activate L-type channels.