ION CHANNELS, RECEPTORS AND SECOND MESSENGERS IN THE NERVOUS SYSTEM

易位后的钙、钠、钾和镁离子 通过离子通道或通过转运蛋白可以引起 释放过程，收缩蛋白，腺苷酸和鸟苷酸环化酶， 磷酸二酯酶、蛋白激酶、磷脂酶、ATP酶等 内切酶 各种类型的受体和各种毒素用于调节 离子通道和第二信使的产生，包括环 核苷酸、二酰基甘油酯、花生四烯酸和磷脂酸。 调制相互作用或“串扰”发生在第二个 信使系统和离子运输系统。 美托毒素a 海洋聚醚增加磷脂分解，导致肌醇 磷酸盐和二环甘油酯的生产。 主要作用部位 似乎是钙离子通道 舞毒蛾毒素反应 被咪唑类有效地封闭， 所谓的钙释放激活钙（CRAC）通道， 当IP 3敏感时， 细胞内钙储存通过受体- 激活磷脂酶C或通过阻断细胞内Ca++- 用毒胡萝卜素检测ATP酶。 然而，其他钙阻滞剂， 河豚毒素应答不阻断ATP或fmLP激活的CRAC通道 在HL-60细胞中。 这些药物包括氟匹立林、五氟利多、洛哌丁胺和 丙二酚 咪唑类（益康唑，咪康唑，SKF 96365， 克霉唑，咪唑啉）不仅阻断美托霉素反应和CRAC 通道，但本身也引起钙的流入。 洛哌丁胺，而 对[Ca 2 +]没有影响;单独，似乎可以增强CRAC通道- 引发了大量涌入 ATP激活HL-60细胞磷脂酰肌醇的降解 通过P2 u受体 在PC 12细胞中，ATP激活磷酸肌醇 通过P2 u和P2 y受体分解。 ATP触发器 PC 12细胞中的钙内流通过另一种P2受体。 激活 P2 y-而不是P2 u-受体导致持续升高 细胞内钙可能通过CRAC通道，激活 钙依赖性钾通道和去甲肾上腺素的释放。

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 breakdown, leading to inositol phosphate and diacyclglyceride production. The primary site of action of maitotoxin appears to be a calcium channel. The maitotoxin-responses are effectively blocked by imidazoles that are also effective in blocking the so-called calcium-release-activated calcium (CRAC) channels, which are activated in plasma membranes of cells when IP3-sensitive intracellular stores of calcium are depleted either through receptor- activation of phospholipase C or through blockade of intracellular Ca++- ATPases by thapsigargin. However, other calcium blockers that prevent maitotoxin-responses do not block CRAC channels activated by ATP or fmLP in HL-60 cells. These include fluspirilene, penfluridol, loperamide and proadifen. The imidazoles (econazole, miconazole, SKF 96365, clotrimazole, calmidazolim) not only block maitotoxin-responses and CRAC channels, but also elicit per se an influx of calcium. Loperamide, while having no effect on [Ca2+]; alone, appears to enhance CRAC channel- elicited influx. ATP activates phosphoinositide breakdown in HL-60 cells through a P2u-receptor. In PC12 cells, ATP activates phosphoinositide breakdown through both P2u and P2y-receptors. In addition, ATP triggers calcium influx in PC12 cells through another P2-receptor. Activation of P2y- but not P2u-receptors leads to a sustained elevation of intracellular calcium presumably via CRAC channels, an activation of calcium-dependent potassium channels and release of norepinephrine.