To be physiologically relevant, the period of the central circadian pacemaker, located in the suprachiasmatic nucleus (SCN), has to match the solar day in a process known as circadian photoentrainment. However, little is known about the spatiotemporal molecular changes that occur in the SCN in response to light. In this study, we sought to systematically characterize the circadian and light effects on activity-dependent markers of transcriptional (cFos), translational (pS6), and epigenetic (pH3) activities in the mouse SCN. To investigate circadian versus light influences on these molecular responses, we harvested brains from adult wild-type mice in darkness at different circadian times (CT) or from mice exposed to a 15-min light pulse at the middle of the subjective day (CT6, no phase shifts), early subjective night (CT14, large phase delays), or late subjective night (CT22, small phase advances). We found that cFos and pS6 exhibited rhythmic circadian expression in the SCN with distinct spatial rhythms, whereas pH3 expression was undetectable at all circadian phases. cFos rhythms were largely limited to the SCN shell, whereas pS6 rhythms encompassed the entire SCN. pH3, pS6, and cFos showed gating in response to light; however, we were surprised to find that the expression levels of these markers were not higher at phases when larger phase shifts are observed behaviorally (CT14 versus CT22). We then used animals lacking melanopsin (melanopsin knockout [MKO]), which show deficits in phase delays, to further investigate whether changes in these molecular markers correspond to behavioral phase shifts. Surprisingly, only pS6 showed deficits in MKOs at CT14. Therefore, our previous understanding of the molecular pathways that lead to circadian photoentrainment needs to be revised.

为了与生理相关，位于视交叉上核 (SCN) 中的中央昼夜节律起搏器的周期必须在称为昼夜节律光夹带的过程中与太阳日相匹配。然而，人们对 SCN 中响应光而发生的时空分子变化知之甚少。在这项研究中，我们试图系统地描述昼夜节律和光对小鼠 SCN 中转录 (cFos)、翻译 (pS6) 和表观遗传 (pH3) 活动的活动依赖性标记的影响。为了研究昼夜节律与光对这些分子反应的影响，我们在不同的昼夜节律时间 (CT) 在黑暗中从成年野生型小鼠或在主观日中间暴露于 15 分钟光脉冲的小鼠 (CT6,无相移），早期主观夜晚（CT14，大相位延迟），或深夜主观（CT22，小阶段推进）。我们发现 cFos 和 pS6 在 SCN 中表现出具有明显空间节律的节律性昼夜节律表达，而在所有昼夜节律阶段都检测不到 pH3 表达。cFos 节律主要限于 SCN 外壳，而 pS6 节律包含整个 SCN。pH3、pS6 和 cFos 显示门控响应光；然而，我们惊讶地发现，在行为上观察到较大的相移时，这些标记的表达水平并不高（CT14 与 CT22）。然后，我们使用缺乏黑视素的动物（黑视素敲除 [MKO]），这些动物显示相位延迟缺陷，以进一步研究这些分子标记的变化是否与行为相移相对应。令人惊讶的是，只有 pS6 在 CT14 时显示出 MKO 缺陷。所以，