Brain energy metabolism actively regulates synaptic transmission and activity. We have previously shown that acute footshock (FS)-stress induces fast and long-lasting functional and morphological changes at excitatory synapses in prefrontal cortex (PFC). Here, we asked whether FS-stress increased energy metabolism in PFC, and modified related cognitive functions. Using positron emission tomography (PET), we found that FS-stress induced a redistribution of glucose metabolism in the brain, with relative decrease of [18F]FDG uptake in ventro-caudal regions and increase in dorso-rostral ones. Absolute [18F]FDG uptake was inversely correlated with serum corticosterone. Increased specific hexokinase activity was also measured in purified PFC synaptosomes (but not in total extract) of FS-stressed rats, which positively correlated with 2-Deoxy [3H] glucose uptake by synaptosomes. In line with increased synaptic energy demand, using an electron microscopy-based stereological approach, we found that acute stress induced a redistribution of mitochondria at excitatory synapses, together with an increase in their volume. The fast functional and metabolic activation of PFC induced by acute stress, was accompanied by rapid and sustained alterations of working memory performance in delayed response to T-maze test. Taken together, the present data suggest that acute stress increases energy consumption at PFC synaptic terminals and alters working memory.

中文翻译：

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急性不可避免的压力迅速增加前额叶皮层的突触能量代谢并改变工作记忆性能。

脑能量代谢积极调节突触传递和活动。先前我们已经表明，急性足底休克（FS）应力在前额叶皮层（PFC）的兴奋性突触处诱导快速且持久的功能和形态变化。在这里，我们问FS压力是否增加了PFC中的能量代谢，并改变了相关的认知功能。使用正电子发射断层扫描（PET），我们发现FS应激诱导了脑内葡萄糖代谢的重新分布，腹侧尾部区域[18F] FDG摄取相对减少，而背侧和鼻背区域的摄取增加。[18F] FDG的绝对摄取与血清皮质酮呈负相关。在FS应激的大鼠中，纯化的PFC突触小体（但未从总提取物中）也测量到比己糖激酶活性的增加，与突触小体对2-脱氧[3H]葡萄糖的摄取呈正相关。符合增加的突触能量需求，使用基于电子显微镜的立体方法，我们发现急性应激诱导兴奋性突触中线粒体的重新分布，并增加了它们的体积。急性应激引起的PFC的快速功能和代谢活化，伴随着对T迷宫测试延迟反应的工作记忆性能的快速持续变化。两者合计，本数据表明，急性应激会增加PFC突触末端的能量消耗并改变工作记忆。我们发现，急性应激会在兴奋性突触中诱导线粒体的重新分布，并增加其体积。急性应激引起的PFC的快速功能和代谢活化，伴随着对T迷宫测试延迟反应的工作记忆性能的快速持续变化。两者合计，本数据表明，急性应激会增加PFC突触末端的能量消耗并改变工作记忆。我们发现，急性应激会在兴奋性突触中诱导线粒体的重新分布，并增加其体积。急性应激引起的PFC的快速功能和代谢活化，伴随着对T迷宫测试延迟反应的工作记忆性能的快速持续变化。两者合计，本数据表明，急性应激会增加PFC突触末端的能量消耗并改变工作记忆。