Sleep Deprivation and Caffeine Treatment Potentiate Photic Resetting of the Master Circadian Clock in a Diurnal Rodent
Sleep Deprivation and Caffeine Treatment Potentiate Photic Resetting of the Master Circadian Clock in a Diurnal Rodent
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DOI：
10.1523/jneurosci.3241-16.2017
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发表时间：
2017-04-19
影响因子：
5.3
通讯作者：
Challet, Etienne
中科院分区：
文献类型：
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作者：
Jha, Pawan Kumar;Bouaouda, Hanan;Challet, Etienne
夜间和昼夜哺乳动物的昼夜节律主要通过光/暗周期与当地时间同步。然而，非光的因素，如行为唤醒和代谢线索，也可以相移主时钟在视交叉上核（SCN）和/或减少夜间啮齿动物的光同步效应。在白天活动的啮齿动物中，唤醒或睡眠不足在这些功能中的作用仍然知之甚少。在本研究中，昼夜苏丹草大鼠，Arvicanthis ansorgei，引起在夜间睡眠剥夺（温和的处理）或咖啡因治疗，都阻止睡眠。分析了从光/暗周期转移到恒定黑暗并在深夜或深夜唤醒的草鼠运动活动的相移。睡眠剥夺导致了一个显著的相位偏移，但在深夜则没有。咖啡因本身不会引起相移。睡眠剥夺和咖啡因治疗增强光诱导的相位延迟和相位提前响应于30分钟的光脉冲，分别。睡眠剥夺在夜间早期，但不是深夜，加强光诱导的c-Fos在腹侧SCN的表达。午夜咖啡因处理触发背侧SCN中的c-Fos表达。睡眠剥夺和咖啡因处理增强光诱导的c-Fos表达在腹侧SCN的calbindincontaining细胞在早期和深夜。这些研究结果表明，在夜间啮齿类动物，行为唤醒诱导的睡眠剥夺或咖啡因在睡眠期间加强光重置的主昼夜节律钟在白天啮齿类动物，和激活的钙结合蛋白含有视交叉上细胞可能参与了这种效果。
Circadian rhythms in nocturnal and diurnal mammals are primarily synchronized to local time by the light/dark cycle. However, nonphotic factors, such as behavioral arousal and metabolic cues, can also phase shift the master clock in the suprachiasmatic nuclei (SCNs) and/or reduce the synchronizing effects of light in nocturnal rodents. In diurnal rodents, the role of arousal or insufficient sleep in these functions is still poorly understood. In the present study, diurnal Sudanian grass rats, Arvicanthis ansorgei, were aroused at night by sleep deprivation (gentle handling) or caffeine treatment that both prevented sleep. Phase shifts of locomotor activity were analyzed in grass rats transferred from a light/dark cycle to constant darkness and aroused in early night or late night. Early night, but not late night, sleep deprivation induced a significant phase shift. Caffeine on its own induced no phase shifts. Both sleep deprivation and caffeine treatment potentiated light-induced phase delays and phase advances in response to a 30 min light pulse, respectively. Sleep deprivation in early night, but not late night, potentiated light-induced c-Fos expression in the ventral SCN. Caffeine treatment in midnight triggered c-Fos expression in dorsal SCN. Both sleep deprivation and caffeine treatment potentiated light-induced c-Fos expression in calbindincontaining cells of the ventral SCN in early and late night. These findings indicate that, in contrast to nocturnal rodents, behavioral arousal induced either by sleep deprivation or caffeine during the sleeping period potentiates light resetting of the master circadian clock in diurnal rodents, and activation of calbindin-containing suprachiasmatic cells may be involved in this effect.