Knox R J, Quattrocki E A, Connor J A, Kaczmarek L K
Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510.
Neuron. 1992 May;8(5):883-9. doi: 10.1016/0896-6273(92)90202-o.
Activation of protein kinase C (PKC) in Aplysia bag cell neurons causes the recruitment of voltage-dependent calcium channels. Using imaging techniques on isolated cells, we have now found that an activator of PKC, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), promotes the rapid appearance of new sites of calcium influx associated with a change in the morphology of neurite endings. In untreated cells, calcium influx triggered by action potentials occurs along neurites and in the central region of growth cones, but does not usually occur at the leading edge of lamellipodia. TPA produces extension of the lamellipodium, and action potentials now trigger calcium influx at the distal edge of the newly extended endings. Cotreatment with TPA and a cyclic AMP analog promotes movement of secretory organelles toward the new sites of calcium influx. Our results suggest that these second messenger systems promote the rapid formation of morphological structures that contribute to the potentiation of peptide release.
海兔（Aplysia）包细胞神经元中蛋白激酶C（PKC）的激活会导致电压依赖性钙通道的募集。利用对分离细胞的成像技术，我们现在发现PKC的激活剂12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）能促进与神经突末端形态变化相关的钙内流新位点的快速出现。在未处理的细胞中，动作电位引发的钙内流沿神经突并在生长锥的中心区域发生，但通常不在片状伪足的前沿发生。TPA会使片状伪足延伸，并且动作电位现在会在新延伸末端的远端边缘引发钙内流。TPA与环磷酸腺苷类似物共同处理会促进分泌细胞器向新的钙内流位点移动。我们的结果表明，这些第二信使系统促进了有助于增强肽释放的形态结构的快速形成。
