ION CHANNELS, RECEPTORS AND SECOND MESSENGERS IN THE NERVOUS SYSTEM

易位后的钙、钠、钾和镁离子 通过离子通道或由运输蛋白引起的激活 释放过程、收缩蛋白、腺苷和鸟苷 环化酶、磷酸二酯酶、蛋白激酶、磷脂酶、三磷酸腺苷酶 和其他酶。各种类型的受体和各种毒素服务于 为了调制离子通道和第二信使的产生，包括 环核苷酸、二酰甘油酯、花生四烯酸和磷脂 酸。调制相互作用或“串扰”发生在 第二信使系统和离子传输系统。 毛霉毒素，一种海洋聚醚，增加磷脂，导致 生产磷酸肌醇和双环甘油酯。主站点 毛霉毒素的作用似乎是一种类似于 对有机化合物对所谓受体的阻断的敏感性- 操作钙(ROC)通道。封锁的效果 多种有机毒素诱导成纤维细胞内钙离子通量 钙通道阻滞剂，包括抗有丝分裂的咪唑 (咪康唑、益康唑等)被推荐为ROC通道阻滞剂，但不 与成纤维细胞中阻滞剂的抗有丝分裂活性有关。 对毛霉毒素诱导的钙流动最有效的阻断剂是 某些含有咪唑、R-维拉帕米和阿米洛利类似物 嘧啶部分上的一种苯基取代基。嗜铬细胞瘤细胞 似乎同时含有ATP和UTP受体，这两种受体都能导致 钙的内流和肌醇磷酸生成的增加。 三磷酸腺苷和三磷酸腺苷类似物，但不是UTP会引发以下后遗症： 细胞内钙的持续升高可能是通过ROC 频道。释放去甲肾上腺素。钙依赖的激活 钾通道。

Calcium, sodium, potassium, and magnesium ions after translocation through ion channels or by transport proteins can cause activation of release processes, contractile proteins, adenylate and guanylate cyclase, phosphodiesterases, protein kinases, phospholipases, ATPases and other enzymes. Receptors of various types and various toxins serve to modulate ion channels and generation of second messengers including cyclic nucleotides, diacylglycerides, arachidonic acid and phosphatidic acid. Modulatory interactions or "cross-talk" occurs both between the second messenger systems and with the ion transport systems. Maitotoxin, a marine polyether increases phospholipid, leading to inositol phosphate and diacyclglyceride production. The primary site of action of maitotoxin appears to be a calcium channel similar in sensitivity to blockade by organic compounds to the so-called receptor- operated calcium (ROC) channels. The efficacy of blockade of maitotoxin-elicited calcium flux in fibroblasts by a variety of organic calcium channel blockers, including the antimitotic imidazoles (miconazole, econazole, etc) proposed as ROC channel blockers, does not correlate with anti-mitotic activity of the blockers in fibroblasts. The most potent blockers for maitotoxin-elicited calcium flux were certain of the imidazoles, R-verapamil and amiloride analogs containing a benzyl substituent on the amidine moiety. Pheochromocytoma cells appear to contain both an ATP and a UTP receptor, both of which lead to an increase in influx of calcium and generation of inositol phosphate. ATP and ATP analogues but not UTP triggers the following sequelae: A sustained elevation of intracellular calcium presumably through ROC channels. Release of norepinephrine. Activation of calcium-dependent potassium channels.