Abstract：
Changes in the amount of daylight (photoperiod) alter physiology and behaviour1,2. Adaptive responses to seasonal photoperiods are vital to all organisms-dysregulation associates with disease, including affective disorders3 and metabolic syndromes4. The circadian rhythm circuitry is implicated in such responses5,6, yet little is known about the precise cellular substrates that underlie phase synchronization to photoperiod change. Here we identify a brain circuit and system of axon branch-specific and reversible neurotransmitter deployment that are critical for behavioural and sleep adaptation to photoperiod. A type of neuron called mrEn1-Pet17 in the mouse brainstem median raphe nucleus segregates serotonin from VGLUT3 (also known as SLC17A8, a proxy for glutamate) to different axonal branches that innervate specific brain regions involved in circadian rhythm and sleep-wake timing8,9. This branch-specific neurotransmitter deployment did not distinguish between daylight and dark phase; however, it reorganized with change in photoperiod. Axonal boutons, but not cell soma, changed neurochemical phenotype upon a shift away from equinox light/dark conditions, and these changes were reversed upon return to equinox conditions. When we genetically disabled Vglut3 in mrEn1-Pet1 neurons, sleep-wake periods, voluntary activity and clock gene expression did not synchronize to the new photoperiod or were delayed. Combining intersectional rabies virus tracing and projection-specific neuronal silencing, we delineated a preoptic area-to-mrEn1Pet1 connection that was responsible for decoding the photoperiodic inputs, driving the neurotransmitter reorganization and promoting behavioural synchronization. Our results reveal a brain circuit and periodic, branch-specific neurotransmitter deployment that regulates organismal adaptation to photoperiod change.
摘要：
日光量（光周期）的变化会改变生理和行为1,2。对季节性光周期的适应性反应对所有生物体-失调与疾病有关，包括情感障碍3和代谢综合征4。昼夜节律电路牵涉到这种反应5,6,但对作为光周期变化的相位同步的基础的精确细胞底物知之甚少。在这里，我们确定了轴突分支特异性和可逆神经递质部署的大脑回路和系统，这对于行为和睡眠适应光周期至关重要。小鼠脑干中缝核中的一种称为mrEn1-Pet17的神经元将来自VGLUT3的5-羟色胺（也称为SLC17A8，是谷氨酸的代用品）分离到不同的轴突分支，这些轴突分支支配了参与昼夜节律和睡眠觉醒的特定大脑区域8,9。这种分支特定的神经递质部署没有区分白天和黑暗阶段;然而，它随着光周期的变化而重组。轴突boutons，但不是细胞瘤，从春分光/暗条件转移后改变了神经化学表型，这些变化在回到春分条件时被逆转。当我们基因禁用mrEn1-Pet1神经元中的Vglut3时，睡眠-觉醒期,自愿活动和时钟基因表达与新的光周期没有同步或延迟。结合交叉狂犬病病毒追踪和投射特异性神经元沉默，我们描绘了一个前视区到mrEn1Pet1的连接，该连接负责解码光周期输入，驱动神经递质重组和促进行为同步。我们的结果揭示了大脑回路和周期性，分支特异性神经递质部署，调节机体对光周期变化的适应。
