Exocytosis in living salivary glands : dynamic analysis by video microscopy and confocal microscopy

大鼠腮腺腺泡细胞具有两种不同的分泌系统，由不同的受体细胞内信号传导机制调节，即，由β-受体介导的酶释放和由α-和毒蕈碱受体触发的液体分泌。先前对固定细胞的光镜和电镜观察表明，β-激动剂引起的胞吐作用导致腔膜扩大，随后通过内吞作用减少，而α-和毒蕈碱激动剂诱导液泡形成，这可能是由高尔基体的一部分肿胀引起的。在用β-激动剂异丙肾上腺素和毒蕈碱激动剂卡巴胆碱刺激期间，用视频增强显微镜和共聚焦显微镜观察活腮腺腺泡细胞表明，与以前的解释相反，异丙肾上腺素引起的胞吐既不涉及管腔膜的总体扩大，也不涉及光显微镜可检测到的内吞作用。这两种膜事件都在卡巴胆碱刺激的细胞中观察到;在这些细胞中形成的“空泡”主要被认为是扩大的管腔。这些结果表明，在唾液分泌系统中存在两种不同的胞吐-胞吞耦合机制。染色的刺激细胞的F-肌动蛋白表明可能参与的微丝和钙在这些不同的膜动力学的歧视。

Rat parotid acinar cells possess two distinct secretion systems regulated by different receptor-intracellular signalling mechanisms, i.e., enzyme release mediated by the beta-receptor and fluid secretion triggered by the alpha- and muscarinic receptors. Previous light and electron microscopic observations on fixed cells have shown that the exocytosis caused by the beta-agonist results in the enlargement of luminal membrane and its subsequent reduction by endocytosis, whereas the alpha- and muscarinic agonists induce vacuole formation that might arise from the swelling of a part of Golgi apparatus. The observation of living parotid acinar cells with video-enhanced microscopy and confocal microscopy during stimulation with the beta-agonist isoproterenol and the muscarinic agonist carbachol have shown that, contrary to the previous interpretations, isoproterenol evoked exocytosis involving neither the gross enlargement of luminal membrane nor the light microscopically detectable endocytosis. Both of these membrane events were instead observed in cells stimulated with carbachol ; the "vacuoles" formed in these cells were considered mostly as the enlarged lumina. These results indicate that two distinct exocytosis-endocytosis coupling mechanisms exist in the salivary secretion system. The staining of the stimulated cells for F-actin suggested the possible involvement of microfilaments and calcium in the discrimination of these different membrane dynamics.