Sattler R, Tymianski M, Feyaz I, Hafner M, Tator C H
Department of Applied Cell Biology, Technical University of Mannheim, Germany.
Brain Res. 1996 May 6;719(1-2):239-46. doi: 10.1016/0006-8993(96)00125-4.
Calcium ion entry following mechanical neurite transection was examined in cultured sympathetic neurons loaded with the Ca2+ indicator fluo-3. Neurite transection produced a rapid [Ca2+]i rise in the cell soma which preceded any [Ca2+]i rise in the neurite (n = 30). Blocking sodium channels with tetrodotoxin had no effect on the Ca2+ rise, but inactivating voltage-sensitive Ca2+ channels by bath-applying 140 mM potassium prior to the transection, and the simultaneous application of nimodipine and omega-conotoxin GVIA, blockers of L-type and N-type Ca2+ channels, respectively, considerably attenuated the Ca2+ rise in the soma and neurites. These data contradict the intuitive hypothesis that Ca2+ entry following mechanical neurite transection occurs via non-specific influx pathways produced by cell-membrane disruption and provide direct evidence in mammalian neurons that immediate, traumatically-induced, increases in neuronal [Ca2+]i are amenable to pharmacological manipulation.
在加载了钙离子指示剂fluo-3的培养交感神经元中，研究了机械性神经突横断后钙离子的内流情况。神经突横断后，细胞体中的[Ca2+]i迅速升高，这早于神经突中任何[Ca2+]i的升高（n = 30）。用河豚毒素阻断钠通道对钙离子升高没有影响，但在横断前通过浴加140 mM钾使电压敏感性钙通道失活，以及同时应用尼莫地平和ω-芋螺毒素GVIA（分别为L型和N型钙通道阻滞剂），可显著减弱细胞体和神经突中的钙离子升高。这些数据与直观的假设相矛盾，即机械性神经突横断后钙离子的内流是通过细胞膜破坏产生的非特异性内流途径发生的，并在哺乳动物神经元中提供了直接证据，表明创伤性诱导的神经元[Ca2+]i的立即增加可通过药物操作进行调节。
