Brain glycolysis (GLY) in the hippocampus (Hipp) plays a critical role in maintaining cognitive functions through energy supply and neuromodulation, mainly via noradrenergic (NA) and serotonergic (5-HT) regulation. However, it is still uncertain whether the occurrence of Hipp GLY depends on neuronal activity. Since running exercise elicits speed-dependent neuronal activation corresponding with energy demand, particularly in the Hipp, we elucidated this issue using a treadmill running model for rats. Rats ran on a treadmill at different speeds (slow: 10 m/min, moderate: 20 m/min, and high: 30 m/min), and were sacrificed using high-power microwave irradiation to detect glycogen, lactate, and monoamine levels in the brain (Hipp, cortex, cerebellum, brainstem etc.) after 30 min of running. Glycogen in the brain, except the hypothalamus, decreased in a speed-dependent manner, which was associated with speed-dependent increased and brain lactate levels. In the Hipp, decreased glycogen and increased lactate were associated with running-speed-dependent activated dopamine (DA), but not NA and 5-HT (Fig. 1A-E). Furthermore, antagonism of DA D2 receptors (not D1) prevented Hipp glycogen decrease during slow running (Fig. 1F). Here we provide the first evidence for neuronal-activity-dependent GLY mediated by DA D2 receptors in the Hipp, suggesting a possible role of DA in exercise-enhanced cognitive functions. $graphic_526FA3B5-3587-4B59-A802-1407F58DE9CB$ Grant Funding Source: This work was supported by JSPS
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