Ozacmak V H, Thorington G U, Fletcher W H, Hessinger D A
Department of Physiology and Pharmacology, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA.
J Exp Biol. 2001 Jun;204(Pt 11):2011-20. doi: 10.1242/jeb.204.11.2011.
Cnidocytes, the stinging cells of cnidarians, optimally discharge nematocysts in response to combined physical contact and stimulation of specific chemoreceptors. In the tentacles of certain sea anemones, the primary chemoreceptors bind N-acetylated sugars, such as N-acetylneuraminic acid (NANA). Sensitization with NANA predisposes contact-sensitive mechanoreceptors (CSMs) to trigger discharge in response to physical contact. In the ectoderm of sea anemone tentacles, cnidocyte/supporting cell complexes (CSCCs) control and trigger nematocyst discharge. Previous findings have implicated cyclic AMP (cAMP) as a second messenger in NANA-sensitized nematocyst discharge. However, no reports have directly demonstrated that the cAMP content of tentacles changes in response to NANA stimulation. We now show that NANA elevates in situ cAMP levels in a dose-dependent manner in the ectoderm of tentacles from the sea anemone Aiptasia pallida. However, the endoderm of tentacles shows no detectable cAMP response to NANA. The effect of NANA on the cAMP content of the ectoderm is biphasic. Micromolar NANA increases the in situ cAMP level, with a maximal response occurring at 1.8x10(-5)mol x l(-1) NANA. At higher NANA concentrations, the cAMP content decreases to that of controls. Because the cAMP dose/response curve to NANA coincides precisely with the dose/response curves of NANA-sensitized nematocyst discharge and nematocyst-mediated adhesive force, a second-messenger role for cAMP in NANA-sensitized nematocyst discharge is strongly suggested. The addition of isobutyl-1-methylxanthine (IBMX) to the medium with sea anemones increases tissue cAMP levels both in the absence and in the presence of NANA. However, anesthetizing anemones in sea water containing high levels of Mg(2+) blocks the NANA-stimulated cAMP response of the ectoderm. In addition, our results suggest that NANA-stimulated cAMP may activate endogenous cAMP-dependent protein kinase (PKA) in broken cell preparations of tentacles. Thus, NANA-stimulated cAMP may function as a second messenger in the NANA chemosensory signaling pathway controlling nematocyst discharge.
刺细胞是刺胞动物的刺细胞，在受到物理接触和特定化学感受器刺激的共同作用时，能最佳地释放刺丝囊。在某些海葵的触手部位，主要的化学感受器会结合N - 乙酰化糖类，比如N - 乙酰神经氨酸（NANA）。用NANA致敏会使接触敏感的机械感受器（CSMs）倾向于在受到物理接触时触发释放。在海葵触手的外胚层中，刺细胞/支持细胞复合体（CSCCs）控制并触发刺丝囊的释放。先前的研究结果表明环磷酸腺苷（cAMP）作为第二信使参与了NANA致敏的刺丝囊释放过程。然而，尚无报道直接证明触手的cAMP含量会因NANA刺激而发生变化。我们现在表明，NANA能使来自苍白艾氏海葵触手外胚层中的原位cAMP水平呈剂量依赖性升高。然而，触手的内胚层对NANA没有可检测到的cAMP反应。NANA对外胚层cAMP含量的影响是双相的。微摩尔浓度的NANA会增加原位cAMP水平，在1.8×10⁻⁵mol·L⁻¹的NANA浓度下出现最大反应。在更高的NANA浓度下，cAMP含量会降至对照水平。由于cAMP对NANA的剂量/反应曲线与NANA致敏的刺丝囊释放及刺丝囊介导的粘附力的剂量/反应曲线精确重合，这强烈表明cAMP在NANA致敏的刺丝囊释放中起第二信使的作用。在含有海葵的培养基中添加异丁基 - 1 - 甲基黄嘌呤（IBMX），无论有无NANA，都会增加组织中的cAMP水平。然而，在含有高浓度Mg²⁺的海水中麻醉海葵会阻断外胚层对NANA刺激的cAMP反应。此外，我们的结果表明，NANA刺激产生的cAMP可能会激活触手破碎细胞制剂中的内源性cAMP依赖性蛋白激酶（PKA）。因此，NANA刺激产生的cAMP可能在控制刺丝囊释放的NANA化学感应信号通路中作为第二信使发挥作用。
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