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

中文翻译：

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激活的 L 型钙通道抑制海葵触手化学敏化的线虫囊排出

由于体内刺细胞排出需要细胞外Ca2+，因此怀疑与Ca2+通道有关；但他们的身份和作用尚未透露。从海葵触角排出的大多数刺丝囊受N-乙酰化糖（例如N-乙酰神经氨酸）致敏化学感受器的控制。激活的化学感受器使接触敏感的机械感受器易于触发放电。我们表明激活 L 型 Ca2+ 通道可抑制 N-乙酰神经氨酸敏化放电，这与先前的建议相反。此外，抑制 L 型通道会增加对 N-乙酰神经氨酸的敏感性。具体来说，我们表明 L 型 Ca2+ 通道激活剂 (-)-Bay K 8644 剂量依赖性地抑制 N-乙酰神经氨酸敏化放电，提高环境 Ca2+ 水平也是如此。我们还表明，降低细胞外 Ca2+ 水平或添加几种选择性和化学上不同的 L 型 Ca2+ 通道阻滞剂中的任何一种，包括二氢吡啶，剂量依赖性地增加 N-乙酰神经氨酸敏感性并拓宽 N-乙酰神经氨酸敏化的动态范围。与这些功能发现一致，苍白球虫表达 L 型 Ca2+ 通道 α 亚基转录本，该转录本编码保守的二氢吡啶结合位点。系统发育分析证实了海葵、珊瑚虫和刺胞动物之间的 Aiptasia Ca2+ 通道 α 亚基序列的密切关系，这些序列延伸到原口和后口双侧。我们得出结论，L 型 Ca2+ 通道活动根据通道活动状态以推拉方式调节 N-乙酰神经氨酸敏化的刺细胞放电。