RECRUITMENT OF CA2+ CHANNELS BY PROTEIN-KINASE-C DURING RAPID FORMATION OF PUTATIVE NEUROPEPTIDE RELEASE SITES IN ISOLATED APLYSIA NEURONS
RECRUITMENT OF CA2+ CHANNELS BY PROTEIN-KINASE-C DURING RAPID FORMATION OF PUTATIVE NEUROPEPTIDE RELEASE SITES IN ISOLATED APLYSIA NEURONS
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DOI：
10.1016/0896-6273(92)90202-o
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发表时间：
1992-05-01
期刊：
影响因子：
16.2
通讯作者：
KACZMAREK, LK
中科院分区：
文献类型：
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作者：
KNOX, RJ;QUATTROCKI, EA;KACZMAREK, LK
海兔袋细胞神经元中蛋白激酶 C (PKC) 的激活导致电压依赖性钙通道的募集。通过对分离细胞进行成像技术，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) 可促进与神经突末端形态变化相关的新钙流入位点的快速出现。在未经处理的细胞中，由动作电位触发的钙流入发生在神经突和生长锥的中心区域，但通常不会发生在板状伪足的前缘。 TPA 产生片状足的延伸，并且动作电位现在触发新延伸末端的远端边缘的钙流入。 TPA 和环 AMP 类似物共同治疗可促进分泌细胞器向钙流入的新位点移动。我们的结果表明，这些第二信使系统促进形态结构的快速形成，从而有助于增强肽的释放。
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.