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

Becausein vivonematocyst discharge requires extracellular Ca2+, Ca(2+)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 forN-acetylated sugars (e.g.,N-acetylneuraminic acid). Activated chemoreceptors predispose contact-sensitive mechanoreceptors to trigger discharge. We show that activating L-type Ca(2+)channels inhibitsN-acetylneuraminic acid-sensitized discharge, contrary to a previous suggestion. In addition, inhibiting L-type channels increases sensitivity toN-acetylneuraminic acid. Specifically, we show that the L-type Ca(2+)channel activator (-)-Bay K 8644 dose-dependently inhibitsN-acetylneuraminic acid-sensitized discharge, as does raising ambient Ca(2+)levels. We also show that lowering extracellular Ca(2+)levels or adding any of several selective and chemically distinct L-type Ca(2+)channel blockers, including dihydropyridines, dose-dependently increasesN-acetylneuraminic acid sensitivity and broadens the dynamic range ofN-acetylneuraminic acid sensitization. Consistent with these functional findings,Aiptasia pallidaexpresses an L-type Ca(2+)channel alpha subunit transcript that encodes a conserved dihydropyridine-binding site. Phylogenetic analysis confirms a close relationship of theAiptasiaCa(2+)channel alpha subunit sequence between anemones, anthozoans, and cnidarians that extends into protostomal and deuterostomal bilaterians. We conclude that L-type Ca(2+)channel activity modulatesN-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 thatN-acetylneuraminic acid chemoreceptor signaling will activate L-type channels.