Tareilus E, Schoch J, Adams M, Breer H
University Stuttgart-Hohenheim, Institute of Zoophysiology, Germany.
Neurochem Int. 1993 Oct;23(4):331-41. doi: 10.1016/0197-0186(93)90077-i.
A combination of the stopped-flow technology with dual channel spectrofluorometry of Ca(2+)-indicators was utilized for the measurement of rapid Ca(2+)-signals in rat cerebral cortical synaptosomes evoked by K(+)-depolarization. There was no observable contribution of Ca(2+)-ions from intracellular stores to the rise in [Ca2+]i. The kinetics of the fast increase in intracellular Ca2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca2+]i and the time course of Ca(2+)-channel inactivation were determined for depolarizations obtained by different extracellular K(+)-concentrations ([K+]o). An apparent threshold was observed at about 18 mM [K+]o; a maximal Ca(2+)-signal amplitude was estimated at about 40 mM [K+]o. Pharmacological properties of the involved Ca(2+)-channels were determined using selective Ca(2+)-channel blockers (Dihydropyridines, omega-Conotoxin, omega-Agatoxins); the results suggest that a P-type voltage-dependent Ca(2+)-channel is the relevant channel type, generating the evoked Ca(2+)-signals in rat cerebral cortical synaptosomes.
将停流技术与Ca(2+)指示剂的双通道荧光光谱法相结合，用于测量K(+)去极化诱发的大鼠大脑皮质突触体中的快速Ca(2+)信号。细胞内储存的Ca(2+)离子对[Ca2+]i升高没有明显贡献。分析了细胞内Ca2+浓度快速升高的动力学与去极化强度的关系。对于不同细胞外K(+)浓度([K+]o)引起的去极化，测定了[Ca2+]i的最大升高和Ca(2+)通道失活的时间进程。在约18 mM [K+]o处观察到一个明显的阈值；在约40 mM [K+]o处估计出最大Ca(2+)信号幅度。使用选择性Ca(2+)通道阻滞剂（二氢吡啶、ω-芋螺毒素、ω-蜘蛛毒素）确定了所涉及的Ca(2+)通道的药理学特性；结果表明，P型电压依赖性Ca(2+)通道是相关的通道类型，在大鼠大脑皮质突触体中产生诱发的Ca(2+)信号。
