ION CHANNELS--RECEPTORS AND SECOND MESSENGERS IN THE NERVOUS SYSTEM

钙、钠、钾和镁离子在 通过离子通道或转运蛋白作为第二转运蛋白进行转位 导致释放过程激活的信使，收缩蛋白， 腺苷和鸟苷环化酶，磷酸二酯酶，蛋白激酶， 磷脂酶、三磷酸腺苷酶等酶。各种类型的受体和 各种毒素调节离子通道和第二代 信使。毛霉毒素(MTX)激活钙摄取和磷脂酰肌醇 在广泛的细胞中分解。这两个反应似乎是 MTX在MTX诱导钙摄取中的独立作用可以是 对甲氨蝶呤诱导的肌醇磷脂无明显抑制作用 崩溃了。需要较低浓度的MTX(下午30分钟)才能诱导 磷脂酰肌醇的分解超过了诱导大量钙的需要 领悟。一种放射性标记的甲氨蝶呤已经制备好，正在进行研究。 约束性研究。在胰岛素瘤细胞中MTX诱导的胰岛素释放 出现的原因是由于以下原因从内部商店释放了@钙质 磷脂酰肌醇三磷酸(IP_3)的分解和生成 )。MTX诱导的胰岛素瘤细胞钙离子内流似乎不是必需的 释放，因为它可以被硝苯地平阻断而不会阻止释放。 值得注意的是，桂利嗪阻止了钙的内流和释放 通过阻断Ip(3)诱导的内源性钙释放来阻断钙的释放。本地 麻醉药增强放射性肌醇在体内的掺入 磷脂显然是通过加强交换途径来实现的。福斯可林和 类似物是神经节细胞烟碱受体的非竞争性阻滞剂 嗜铬细胞瘤细胞中的通道复合体，但不像其他非嗜铬细胞瘤细胞 竞争性阻滞剂不会增强脱敏作用。不可逆转的局部性 麻醉剂异硫氰酸丙卡因抑制放射性物质的结合 巴曲霉毒素对钠通道的作用比抑制作用大得多 巴曲霉毒素引起的钠通量，表明钠大量过剩 突触神经体中的通道超出了诱导最大 高岭土的涌入。

Calcium, sodium, potassium, and magnesium, ions can serve after translocation through ion channels or by transport proteins as second messengers to cause activation of release processes, contractile proteins, adenylate and guanylate cyclase, phosphodiesterases, protein kinases, phospholipases, ATPases and other enzymes. Receptors of various types an various toxins serve to modulate ion channels and generation of second messengers. Maitotoxin (MTX) activates calcium uptake and phosphoinositide breakdown in a wide range of cells. The two responses appear to be independent actions of MTX in that MTX-elicited calcium uptake can be greatly inhibited with no effort on MTX-elicited phosphoinositide breakdown. Lower concentrations of MTX (30 pM) are required to elicit phosphoinositide breakdown than are required to elicit significant calcium uptake. A radiolabelled MTX has been prepared and is being investigated in binding studies. In insulinoma cells MTX-elicited release of insulin appears due to release of @calcium from internal stores as a result of phosphoinositide breakdown and Generation of inositol trisphosphate (IP 3 ). MTX-elicited influx of calcium in insulinoma cells appears nonessential to release since it can be blocked by nifedipine without blocking release. Remarkably, cinnarizine blocks calcium influx and release it appears to block release by blocking Ip(3)-induced release of internal calcium. Local anesthetics enhance incorporation of radioactive inositol into phospholipids apparently by enhancing an exchange pathway. Forskolin and analogs are noncompetitive blockers of ganglionic nicotinic receptor channel complexes in pheochromocytoma cells, but unlike other non- competitive blockers do not enhance desensitization. An irreversible local anesthetic, proparacaine isothiocyanate, inhibits binding of a radioactive batrachotoxin to sodium channels to a much granter extent than inhibition of batrachotoxin-elicited sodium flux, indicating a large excess of sodium channels in synaptoneurosomes beyond those needed to induce a maximal influx of sorlium.