Nguyen Michael P, Bittner George D, Fishman Harvey M
Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas.
J Neurosci Res. 2005 Sep 15;81(6):805-16. doi: 10.1002/jnr.20606.
Nerve cells may survive or die after axonal or dendritic transection. After neurite transection near (<50 mum) the cell body of Fura-2-loaded B 104 neuroblastoma (rat brain-derived) cells, the somal calcium concentration (SCC) undergoes a three-phase transient change: a rapid (0-0.15-min post-transection [PT]) rise phase, followed by an early (0.15--1.5-min PT) rapid decay phase, and succeeded by a late (1.5-60-min PT) slower decay phase that restores SCC to preinjury levels. The SCC in a critical interval (1.5-12.5 min PT) of the third transient phase correlates with cell fate, i.e., most transected cells that exclude dye (restore a barrier) and die have a significantly higher (P<0.005) SCC in this critical interval than do transected cells that exclude dye and survive at 24-hr PT. Loading BAPTA (chelation of somal Ca(2+)) before, but not after, the critical interval increases the percentage of cells that survive compared to that of cells transected without BAPTA loading. Furthermore, most transected cells that die despite successful barrier restoration exhibit characteristics consistent with apoptosis initiated during the critical interval of the SCC, including caspase activation and plasmalemmal phosphatidylserine translocation. These data suggest that decreased cell survival for injuries near the soma is due to Ca(2+)-initiated apoptosis during the critical interval of the third phase of the SCC transient. (c) 2005 Wiley-Liss, Inc.
轴突或树突横断后，神经细胞可能存活或死亡。在装载Fura-2的B104神经母细胞瘤（源自大鼠脑）细胞的细胞体附近（<50μm）进行神经突横断后，胞体钙浓度（SCC）经历三相瞬态变化：快速（横断后0 - 0.15分钟[PT]）上升期，随后是早期（0.15 - 1.5分钟PT）快速衰减期，接着是晚期（1.5 - 60分钟PT）较慢衰减期，该期将SCC恢复到损伤前水平。第三相瞬态的关键间隔（1.5 - 12.5分钟PT）内的SCC与细胞命运相关，即大多数排斥染料（恢复屏障）并死亡的横断细胞在这个关键间隔内的SCC显著高于（P<0.005）在24小时PT时排斥染料并存活的横断细胞。在关键间隔之前而非之后加载BAPTA（螯合胞体Ca(2+)）与未加载BAPTA横断的细胞相比，增加了存活细胞的百分比。此外，尽管成功恢复屏障但仍死亡的大多数横断细胞表现出与在SCC关键间隔期间启动的凋亡一致的特征，包括半胱天冬酶激活和质膜磷脂酰丝氨酸易位。这些数据表明，胞体附近损伤导致的细胞存活率降低是由于SCC瞬态第三相关键间隔期间Ca(2+)引发的凋亡。(c) 2005 Wiley-Liss, Inc.
