Huang L Y, Neher E
Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77555-1069, USA.
Neuron. 1996 Jul;17(1):135-45. doi: 10.1016/s0896-6273(00)80287-1.
Using capacitance measurements and the single-cell immunoblot assay to study secretion in dorsal root ganglion neurons, we found that the somata underwent robust exocytosis upon depolarization and released substance P, in response to KCl stimulation. The parallel changes between capacitance responses and intracellular Ca2+ concentration ([Ca2+]i) at different membrane potentials and the inhibition of exocytosis by Ca2+ chelators suggest that soma release is Ca(2+)-dependent. We also assessed the level of Ca2+ required for exocytosis by raising the average [Ca2+]i with the Ca2+ ionophore, ionomycin. Capacitance changes were triggered by cytosolic Ca2+ > 0.6 microM; the [Ca2+]i at the release sites during depolarizations was estimated to be 3-10 microM. These Ca2+ levels are similar to those obtained from neuroendocrine cells, but are at least 10 times lower than those required for transmitter release from nerve terminals.
我们使用电容测量和单细胞免疫印迹分析来研究背根神经节神经元的分泌，发现胞体在去极化时会发生强烈的胞吐作用，并在氯化钾刺激下释放P物质。在不同膜电位下，电容反应与细胞内钙离子浓度（[Ca2+]i）之间的平行变化以及钙离子螯合剂对胞吐作用的抑制表明，胞体释放是钙离子依赖性的。我们还通过使用钙离子载体离子霉素提高平均[Ca2+]i来评估胞吐作用所需的钙离子水平。胞质钙离子>0.6微摩尔触发电容变化；去极化期间释放位点的[Ca2+]i估计为3-10微摩尔。这些钙离子水平与从神经内分泌细胞获得的水平相似，但比神经末梢释放递质所需的水平至少低10倍。
