Like other cnidarians, the freshwater organism Hydra is characterized by the possession of cnidocytes (stinging cells). Most cnidocytes are located on hydra tentacles, where they are organized along with sensory cells and ganglion cells into battery complexes. The function of the battery complexes is to integrate multiple types of stimuli for the regulation of cnidocyte discharge. The molecular mechanisms controlling the discharge of cnidocytes are not yet fully understood, but it is known that discharge depends on extracellular Ca²⁺ and that mechanically induced cnidocyte discharge can be enhanced by the presence of prey extracts and other chemicals. Experiments in this paper show that a PKD2 (polycystin 2) transient receptor potential (TRP) channel is expressed in hydra tentacles and bases. PKD2 (TRPP) channels belong to the TRP channel superfamily and are non-selective Ca²⁺ channels involved in the transduction of both mechanical and chemical stimuli in other organisms. Non-specific PKD2 channel inhibitors Neo (neomycin) and Gd³⁺ (gadolinium) inhibit both prey capture and cnidocyte discharge in hydra. The PKD2 activator Trip (triptolide) enhances cnidocyte discharge in both starved and satiated hydra and reduces the inhibition of cnidocyte discharge caused by Neo. PKD1 and 2 proteins are known to act together to transduce mechanical and chemical stimuli; in situ hybridization experiments show that a PKD1 gene is expressed in hydra tentacles and bases, suggesting that polycystins play a direct or indirect role in cnidocyte discharge.

中文翻译：

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有证据表明，多囊藻毒素参与了九头蛇血红细胞的释放。

像其他cnidarians一样，淡水生物Hydra的特征是拥有cnidocytes（刺细胞）。大多数的小胶质细胞位于水hydr触角上，在那里它们与感觉细胞和神经节细胞一起组织成电池复合体。电池复合物的功能是整合多种刺激物，以调节小胶质细胞的放电。尚不完全了解控制小胶质细胞释放的分子机制，但已知释放取决于细胞外Ca ²⁺猎物提取物和其他化学物质的存在可以增强机械诱导的软骨细胞放电。本文的实验表明，在水触角和碱基中表达了PKD2（多囊藻蛋白2）瞬时受体电位（TRP）通道。PKD2（TRPP）通道属于TRP通道超家族，是非选择性Ca ²⁺通道，参与其他生物体的机械和化学刺激的转导。非特异性PKD2通道抑制剂Neo（neomycin）和Gd ³⁺（ga）抑制水中的猎物捕获和少突胶质细胞释放。PKD2激活剂Trip（雷公藤甲素）可增强饥饿和饱腹水肿中的小胶质细胞放电，并减少Neo引起的小胶质细胞放电抑制作用。已知PKD1和2蛋白共同起作用，以转导机械和化学刺激。原位杂交实验表明，PKD1基因在水触角和碱基中表达，表明多囊藻毒素在小胶质细胞的放电中起直接或间接的作用。