The effects of dihydropyridines on neurotransmitter release from cultured neuronal cells.
The effects of dihydropyridines on neurotransmitter release from cultured neuronal cells.
复制标题
二氢吡啶对培养神经元细胞释放神经递质的影响。
DOI：
10.1016/0024-3205(84)90100-0
复制
发表时间：
1984
期刊：
影响因子：
6.1
通讯作者：
Miller,RJ
中科院分区：
文献类型：
--
作者：
Shalaby,IA;Kongsamut,S;Freedman,SB;Miller,RJ
去极化刺激增加释放的递质物质从培养的PC 12嗜铬细胞瘤细胞和重新聚集培养的小鼠中脑多巴胺神经元。我们分别测定了（3 H）去甲肾上腺素和（3 H）多巴胺从这些系统的刺激释放。在培养的小鼠多巴胺能神经元中，几种有机钙通道阻滞剂，包括尼群地平，D-600，维拉帕米和地尔硫卓不能抑制钾诱发的递质释放。然而，释放被3 mM钴阻断。新型二氢吡啶类钙通道激动剂BAY K8644对基础或诱发的多巴胺释放也没有影响。相反，BAY K8644极大地刺激钾诱发的PC 12细胞释放（3 H）去甲肾上腺素。BAY K8644的促释作用可被二氢吡啶类拮抗剂尼群地平阻断。这些结果表明，虽然刺激分泌耦合在PC 12细胞系涉及二氢吡啶敏感的钙通道，这是不是在原代培养的神经元的情况。
Depolarizing stimuli increase the release of transmitter substances from cultured PC12 pheochromocytoma cells and reaggregate cultures of mouse mesencephalic dopamine neurones. We measured the stimulated release of (3H) norepinephrine and (3H) dopamine from these systems respectively. In the cultured mouse dopaminergic neurones, several organic calcium channel blockers including nitrendipine, D-600, verapamil and diltiazem were unable to inhibit potassium-evoked transmitter release. However, release was blocked by 3 mM cobalt. The novel dihydropyridine calcium channel agonist BAY K8644 also had no effect on basal or evoked dopamine release. In contrast, BAY K8644 greatly stimulated the potassium-evoked release of (3H) norepinephrine from PC12 cells. The BAY K8644 enhanced release could be blocked by the dihydropyridine antagonist nitrendipine. These results indicate that while stimulus-secretion coupling in the PC12 cell line involves dihydropyridine sensitive calcium channels, this is not the case in primary cultured neurones.