Metabolic adaptation is a critical feature of synaptic plasticity. Indeed, synaptic plasticity requires the utilization and resupply of metabolites, in particular when the turnover is high and fast such as in stress conditions. What accounts for the localized energy burden of the post-synaptic compartment to the build up of chronic stress is currently not understood. We used in vivo microscopy of genetically encoded fluorescent probes to track changes of mitochondria, dendritic spines, ATP and H2O2 levels in pyramidal neurons of cortex before and after chronic unpredictable mild stress. Data revealed hotspots of postsynaptic mitochondria and dendritic spine turnover. Pharmacogenetic approach to force expression of the metabolic stress gene NR4A1 caused the fragmentation of postsynaptic mitochondria and loss of proximal dendritic spine clusters, whereas a dominant-negative mutant counteracted the effect of chronic stress. When fragmented, dendritic mitochondria produced lesser ATP at resting state and more on acute demand. This corresponded with significant production of mitochondrial H2O2 oxidative species in the dendritic compartment. Together, data indicate that pyramidal neurons adjust proximal dendritic spine turnover and mitochondria functions in keeping with synaptic demands.

代谢适应是突触可塑性的一个关键特征。事实上，突触可塑性需要代谢物的利用和再供给，特别是当周转率高且快时，例如在压力条件下。目前尚不清楚是什么解释了突触后隔室的局部能量负担与慢性压力的积累。我们使用基因编码荧光探针的体内显微镜检查来跟踪在慢性不可预测的轻度压力之前和之后皮质锥体神经元中线粒体、树突棘、ATP 和 H2O2 水平的变化。数据揭示了突触后线粒体和树突棘转换的热点。强制表达代谢应激基因NR4A1 的药物遗传学方法导致突触后线粒体的断裂和近端树突棘簇的丢失，而显性失活突变体抵消了慢性压力的影响。当碎片化时，树突状线粒体在静止状态下产生较少的 ATP，在急性需求时产生更多。这与树突隔室中线粒体 H2O2 氧化物质的大量产生相对应。总之，数据表明锥体神经元根据突触需求调整近端树突棘周转和线粒体功能。