Circadian regulation of food-anticipatory activity in molecular clock-deficient mice.
Circadian regulation of food-anticipatory activity in molecular clock-deficient mice.
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DOI：
10.1371/journal.pone.0048892
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Nakamura W
中科院分区：
文献类型：
--
作者：
Takasu NN;Kurosawa G;Tokuda IT;Mochizuki A;Todo T;Nakamura W
在哺乳动物大脑中，下丘脑前部的视交叉上核（SCN）被认为是主要的昼夜节律起搏器，在光/暗周期的基础上保持大多数生理和行为过程的节律。由于食物供应限制在一天中的某个时间，即使在SCN消融后也会激发预期行为，因此这种行为被认为是在另一个昼夜节律振荡器的控制下。然而，根据最近的研究，缺乏昼夜节律钟功能的突变小鼠表现出正常的食物预期活动（FAA），即在周期性进食之前每天增加运动活动，这表明FAA独立于已知的昼夜节律振荡器。为了研究FAA的分子基础，我们研究了缺乏分子钟成分的小鼠的振荡特性。SCN病变或突变昼夜节律周期的小鼠暴露于昼夜节律范围内和昼夜节律范围外的限制性喂养时间表。周期性喂养导致夹带FAA的节奏只在有限的昼夜节律范围内。Cry 1 −/−小鼠被认为是一种“短期突变体”，其喂养周期比Cry 2 −/−小鼠短。这一结果表明，FAA节律的固有周期也受到Cry缺乏的影响。缺乏分子钟机制另一个基本元素的Bmal 1 −/−小鼠，在进食前表现出远离昼夜节律范围的活动增加，表明昼夜节律振荡不足。我们建议，小鼠具有食物耐受的起搏器以外的SCN，其中典型的时钟基因，如Cry 1，Cry 2和Bmal 1发挥重要作用，在调节FAA的昼夜振荡的方式。
In the mammalian brain, the suprachiasmatic nucleus (SCN) of the anterior hypothalamus is considered to be the principal circadian pacemaker, keeping the rhythm of most physiological and behavioral processes on the basis of light/dark cycles. Because restriction of food availability to a certain time of day elicits anticipatory behavior even after ablation of the SCN, such behavior has been assumed to be under the control of another circadian oscillator. According to recent studies, however, mutant mice lacking circadian clock function exhibit normal food-anticipatory activity (FAA), a daily increase in locomotor activity preceding periodic feeding, suggesting that FAA is independent of the known circadian oscillator. To investigate the molecular basis of FAA, we examined oscillatory properties in mice lacking molecular clock components. Mice with SCN lesions or with mutant circadian periods were exposed to restricted feeding schedules at periods within and outside circadian range. Periodic feeding led to the entrainment of FAA rhythms only within a limited circadian range. Cry1−/− mice, which are known to be a “short-period mutant,” entrained to a shorter period of feeding cycles than did Cry2−/− mice. This result indicated that the intrinsic periods of FAA rhythms are also affected by Cry deficiency. Bmal1 −/− mice, deficient in another essential element of the molecular clock machinery, exhibited a pre-feeding increase of activity far from circadian range, indicating a deficit in circadian oscillation. We propose that mice possess a food-entrainable pacemaker outside the SCN in which canonical clock genes such as Cry1, Cry2 and Bmal1 play essential roles in regulating FAA in a circadian oscillatory manner.
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