The mechanisms underlying the mammalian ultradian sleep rhythm—the alternation of rapid-eye-movement (REM) and slow-wave (SW) states—are not well understood but probably depend, at least in part, on circuits in the brainstem^1,2,3,4,5,6. Here, we use perturbation experiments to probe this ultradian rhythm in sleeping lizards (Pogona vitticeps)^7,8,9 and test the hypothesis that it originates in a central pattern generator^10,11—circuits that are typically susceptible to phase-dependent reset and entrainment by external stimuli¹². Using light pulses, we find that Pogona’s ultradian rhythm⁸ can be reset in a phase-dependent manner, with a critical transition from phase delay to phase advance in the middle of SW. The ultradian rhythm frequency can be decreased or increased, within limits, by entrainment with light pulses. During entrainment, Pogona REM (REM_P) can be shortened but not lengthened, whereas SW can be dilated more flexibly. In awake animals, a few alternating light/dark epochs matching natural REM_P and SW durations entrain a sleep-like brain rhythm, suggesting the transient activation of an ultradian rhythm generator. In sleeping animals, a light pulse delivered to a single eye causes an immediate ultradian rhythm reset, but only of the contralateral hemisphere; both sides resynchronize spontaneously, indicating that sleep is controlled by paired rhythm-generating circuits linked by functional excitation. Our results indicate that central pattern generators of a type usually known to control motor rhythms may also organize the ultradian sleep rhythm in a vertebrate.

哺乳动物超离子睡眠节律的潜在机制——快速眼动 （REM） 和慢波 （SW） 状态的交替——尚不清楚，但可能至少部分取决于脑干中的回路^1,2,3,4,5,6。在这里，我们使用扰动实验来探测睡蜥蜴 （Pogona vitticeps） ^7,8,9 的这种超节律，并检验它起源于中央模式发生器^10,11 的假设——这些电路通常容易受到相位依赖性复位和外部刺激的夹带¹²。使用光脉冲，我们发现 Pogon 的 ultradian rhythm⁸ 可以以相位依赖性方式重置，在 SW 中间从相位延迟到相位提前的关键过渡。超节律频率可以在一定范围内通过光脉冲夹带而降低或增加。在夹带过程中，Pogona REM （REM_P） 可以缩短但不能延长，而 SW 可以更灵活地扩张。在清醒的动物中，一些与自然 REM_P 和 SW 持续时间相匹配的交替亮/暗时期会带来类似睡眠的大脑节律，这表明超节律发生器的瞬时激活。在睡眠动物中，传递到单眼的光脉冲会立即导致超音节律重置，但仅限于对侧半球;两侧自发地重新同步，表明睡眠是由功能兴奋连接的成对节律产生回路控制的。我们的结果表明，通常已知的控制运动节律的中央模式生成器也可能组织脊椎动物的超离子睡眠节律。