Shalaby I A, Kongsamut S, Freedman S B, Miller R J
Life Sci. 1984 Sep 17;35(12):1289-95. doi: 10.1016/0024-3205(84)90100-0.
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.
去极化刺激可增加培养的PC12嗜铬细胞瘤细胞中递质的释放，并使小鼠中脑多巴胺神经元的培养物重新聚集。我们分别测量了这些系统中（3H）去甲肾上腺素和（3H）多巴胺的刺激释放。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、维拉帕米和地尔硫䓬，均无法抑制钾离子诱发的递质释放。然而，3 mM的钴可阻断释放。新型二氢吡啶钙通道激动剂BAY K8644对基础或诱发的多巴胺释放也没有影响。相比之下，BAY K8644极大地刺激了PC12细胞中钾离子诱发的（3H）去甲肾上腺素释放。BAY K8644增强的释放可被二氢吡啶拮抗剂尼群地平阻断。这些结果表明，虽然PC12细胞系中的刺激-分泌偶联涉及对二氢吡啶敏感的钙通道，但原代培养的神经元并非如此。
