Circadian clocks play key roles in how organisms respond to and even anticipate seasonal change in day length, or photoperiod. In mammals, photoperiod is encoded by the central circadian pacemaker in the brain, the suprachiasmatic nucleus (SCN). The subpopulation of SCN neurons that secrete the neuropeptide VIP mediates the transmission of light information within the SCN neural network, suggesting a role for these neurons in circadian plasticity in response to light information that has yet to be directly tested. Here, we used in vivo optogenetic stimulation of VIPergic SCN neurons followed by ex vivo PERIOD 2::LUCIFERASE (PER2::LUC) bioluminescent imaging to test whether activation of this SCN neuron subpopulation can induce SCN network changes that are hallmarks of photoperiodic encoding. We found that optogenetic stimulation designed to mimic a long photoperiod indeed altered subsequent SCN entrained phase, increased the phase dispersal of PER2 rhythms within the SCN network, and shortened SCN free-running period—similar to the effects of a true extension of photoperiod. Optogenetic stimulation also induced analogous changes on related aspects of locomotor behaviour in vivo. Thus, selective activation of VIPergic SCN neurons induces photoperiodic network plasticity in the SCN that underpins photoperiodic entrainment of behaviour.

中文翻译：

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VIPergic SCN 神经元的光遗传学刺激诱导哺乳动物生物钟的光周期样变化

生物钟在生物体如何响应甚至预测昼长或光周期的季节性变化方面发挥着关键作用。在哺乳动物中，光周期由大脑中的中央昼夜节律起搏器，即视交叉上核 (SCN) 编码。分泌神经肽 VIP 的 SCN 神经元亚群介导 SCN 神经网络内光信息的传递，表明这些神经元在响应尚未直接测试的光信息的昼夜节律可塑性中发挥作用。在这里，我们使用了 VIPergic SCN 神经元的体内光遗传学刺激，然后是离体 PERIOD 2::LUCIFERASE (PER2::LUC) 生物发光成像，以测试该 SCN 神经元亚群的激活是否可以诱导作为光周期编码标志的 SCN 网络变化。我们发现，旨在模拟长光周期的光遗传学刺激确实改变了随后的 SCN 夹带相位，增加了 SCN 网络内 PER2 节律的相位扩散，并缩短了 SCN 自由运行期——类似于真正延长光周期的效果。光遗传学刺激还引起体内运动行为相关方面的类似变化。因此，VIPergic SCN 神经元的选择性激活会诱导 SCN 中的光周期网络可塑性，从而支持光周期行为。光遗传学刺激还引起体内运动行为相关方面的类似变化。因此，VIPergic SCN 神经元的选择性激活会诱导 SCN 中的光周期网络可塑性，从而支持光周期行为。光遗传学刺激还引起体内运动行为相关方面的类似变化。因此，VIPergic SCN 神经元的选择性激活会诱导 SCN 中的光周期网络可塑性，从而支持光周期行为。