Department of Clinical Sciences Lund, Laboratory for Experimental Brain Research, Lund University, Lund, Sweden.
J Cereb Blood Flow Metab. 2011 Aug;31(8):1663-7. doi: 10.1038/jcbfm.2011.37. Epub 2011 Apr 6.
Neuronal endoplasmic reticulum (ER), continuous from soma to dendritic spines, undergoes rapid fragmentation in response to N-methyl-D-aspartate (NMDA) receptor stimulation in hippocampal slices and neuronal primary cultures. Here, we show that ER fragments in the mouse brain following cardiac arrest (CA) induced brain ischemia. The ER structure was assessed in vivo in cortical pyramidal neurons in transgenic mice expressing ER-targeted GFP using two-photon laser scanning microscopy with fluorescence recovery after photobleaching (FRAP). Endoplasmic reticulum fragmentation occurred 1 to 2 minutes after CA and once induced, fragmentation was rapid (<15 seconds). We propose that acute ER fragmentation may be a protective response against severe ischemic stress.
神经元内质网(ER)从体部延伸到树突棘,在海马切片和神经元原代培养物中,对内质网 NMDA 受体刺激会迅速发生碎片化。在这里,我们显示在心脏骤停(CA)诱导的脑缺血后,小鼠大脑中的 ER 片段。使用双光子激光扫描显微镜和荧光漂白后恢复(FRAP),在表达 ER 靶向 GFP 的转基因小鼠的皮质锥体神经元中评估体内 ER 结构。CA 后 1 至 2 分钟发生内质网碎片化,一旦发生,碎片化速度很快(<15 秒)。我们提出,急性内质网碎片化可能是对严重缺血应激的一种保护反应。