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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Actin redistribution underlies the sparing effect of mild hypothermia on dendritic spine morphology after in vitro ischemia.
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Actin redistribution underlies the sparing effect of mild hypothermia on dendritic spine morphology after in vitro ischemia.

机译：肌动蛋白的再分配是轻度低温对体外缺血后树突棘形态的保护作用的基础。

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Brain hypothermia is at present the most effective neuroprotective treatment against brain ischemia in man. Ischemia induces a redistribution of proteins involved in synaptic functions, which is markedly diminished by therapeutic hypothermia (33 degrees C). Dendritic spines at excitatory synapses are motile and show both shape changes and rearrangement of synaptic proteins as a consequence of neuronal activity. We investigated the effect of reduced temperature (33 degrees C and 27 degrees C compared with 37 degrees C), on spine motility, length and morphology by studying the distribution of GFP-actin before, during and after induction of in vitro ischemia. Because high-concentration actin filaments are located inside spines, dissociated hippocampal neurons (7-11 DIV) from transgenic mice expressing GFP-actin were used in this study. The movement of the spines and the distribution of GFP-actin were recorded using time-lapse fluorescence microscopy. Under normal conditions rapid rearrangement of GFP-actin was seen in dendritic spines, indicating highly motile spines at 37 degrees C. Decreasing the incubation temperature to 33 degrees C or 27 degrees C, dramatically reduces actin dynamics (spine motility) by approximately 50% and 70%, respectively. In addition, the length of the spine shaft was reduced by 20%. We propose that decreasing the temperature from 37 degrees C to 33 degrees C during ischemia decreases the neuronal actin polymerization rate, which reduces spine calcium kinetics, disrupts detrimental cell signaling and protects neurons against damage.
机译：脑低温是目前针对人脑缺血最有效的神经保护疗法。缺血诱导突触功能所涉及的蛋白质的重新分布，治疗性低温（33摄氏度）明显降低了这种分布。兴奋性突触处的树突棘是活动的，并且由于神经元活性而显示出突触蛋白的形状变化和重排。我们通过研究GFP-肌动蛋白在体外缺血诱导之前，之中和之后的分布，研究了温度降低（33摄氏度和27摄氏度，而37摄氏度相比37摄氏度）对脊柱运动性，长度和形态的影响。由于高浓度肌动蛋白丝位于棘突内部，因此在本研究中使用了来自表达GFP-肌动蛋白的转基因小鼠的海马神经元解离（7-11 DIV）。使用延时荧光显微镜记录棘的运动和GFP-肌动蛋白的分布。在正常情况下，在树突棘中观察到GFP-肌动蛋白的快速重排，表明棘突棘在37摄氏度时具有很高的运动能力。将孵育温度降低到33摄氏度或27摄氏度时，肌动蛋白动力学（脊柱运动性）显着降低了约50％分别为70％。此外，脊柱的长度减少了20％。我们建议在缺血期间将温度从37摄氏度降低到33摄氏度会降低神经元肌动蛋白的聚合速率，从而降低脊柱钙动力学，破坏有害的细胞信号传导并保护神经元免受损伤。

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