It has been suggested that, in states of arousal, release of noradrenaline and β-adrenergic signalling affect long-term memory formation by stimulating astrocytic lactate production from glycogen. However, the temporal relationship between cortical activity and cellular lactate fluctuations upon changes in arousal remains to be fully established. Also, the role of β-adrenergic signalling and brain glycogen metabolism on neural lactate dynamics in vivo is still unknown. Here, we show that an arousal-induced increase in cortical activity triggers lactate release into the extracellular space, and this correlates with a fast and prominent lactate dip in astrocytes. The immediate drop in astrocytic lactate concentration and the parallel increase in extracellular lactate levels underline an activity-dependent lactate release from astrocytes. Moreover, when β-adrenergic signalling is blocked or the brain is depleted of glycogen, the arousal-evoked cellular lactate surges are significantly reduced. We provide in vivo evidence that cortical activation upon arousal triggers lactate release from astrocytes, a rise in intracellular lactate levels mediated by β-adrenergic signalling and the mobilization of lactate from glycogen stores.

已经提出，在觉醒状态下，去甲肾上腺素的释放和β-肾上腺素能信号传导通过刺激糖原中星形胶质乳酸的产生影响长期记忆的形成。然而，皮层活动和唤醒引起的细胞乳酸波动之间的时间关系仍有待完全建立。同样，β-肾上腺素信号传导和脑糖原代谢对体内神经乳酸动力学的作用仍是未知的。在这里，我们表明唤醒引起的皮质活动的增加触发乳酸释放到细胞外空间，并且这与星形胶质细胞中乳酸的快速浸润相关。星形胶质细胞乳酸浓度的立即下降和细胞外乳酸水平的平行增加强调了星形胶质细胞活性依赖的乳酸释放。此外，当β-肾上腺素能信号传导受阻或大脑中的糖原消耗，尽时，唤起的细胞乳酸盐激增会大大降低。我们提供体内证据，唤醒后皮质激活触发星形胶质细胞释放乳酸，β-肾上腺素能信号传导介导的细胞内乳酸水平升高以及糖原存储中乳酸的动员。