Tomita Jun, Ban Gosuke, Kato Yoshiaki S, Kume Kazuhiko
Department of Neuropharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Front Neurosci. 2021 Oct 15;15:647117. doi: 10.3389/fnins.2021.647117. eCollection 2021.
The central complex is one of the major brain regions that control sleep in . However, the circuitry details of sleep regulation have not been elucidated yet. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the and the PB columnar neurons with - promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contact between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. () knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB, regulated by dopamine signaling, mediates sleep-wakefulness.
中央复合体是控制睡眠的主要脑区之一。然而，睡眠调节的神经回路细节尚未阐明。在这里，我们展示了中央复合体原脑桥（PB）中一种新的睡眠调节神经元回路。用[具体标记物]标记的PB中间神经元和用[具体标记物]标记的PB柱状神经元的激活分别促进了睡眠和觉醒。跨突触伙伴的靶向绿色荧光蛋白重组（t-GRASP）分析表明这两组睡眠调节PB神经元之间存在突触联系。此外，我们发现投射到PB的一对多巴胺能（DA）神经元（T1 DA神经元）的激活会减少睡眠。促进觉醒的T1 DA神经元与促进睡眠的PB中间神经元形成紧密联系。在促进睡眠的PB中间神经元中敲低[具体基因]会增加睡眠。这些结果表明，受多巴胺信号调节的PB中的神经元回路介导了睡眠-觉醒。
