] indicate that sleep bout durations exhibit an exponential distribution, whereas wake bout durations exhibit a power-law distribution. Moreover, it was found that wake bout distributions, but not sleep bout distributions, exhibit scale invariance across mammals of different body sizes. Here we test the generalizability of these findings by examining the distributions of sleep and wake bout durations in infant rats between 2 and 21 days of age. In agreement with Lo et al., we find that sleep bout durations exhibit exponential distributions at all ages examined. In contrast, however, wake bout durations also exhibit exponential distributions at the younger ages, with a clear power-law distribution only emerging at the older ages. Further analyses failed to find substantial evidence either of short-or long-term correlations in the data, thus suggesting that the durations of current sleep and wake bouts evolve through time without memory of the durations of preceding bouts. These findings further support the notion that bouts of sleep and wakefulness are regulated independently. Moreover, in light of recent evidence that developmental changes in sleep and wake bouts can be attributed in part to increasing forebrain influences, these findings suggest the possibility of identifying specific neural circuits that modulate the changing complexity of sleep and wake dynamics during development.atonia ͉ renewal process ͉ Markov process ͉ development A s members of a diurnal species, adult humans experience sleep as a prolonged period of rest during the night; however, sleep actually occurs as a series of discrete bouts interrupted by bouts of wakefulness. What is perhaps most striking during the first several months after birth, when circadian influences on behavioral state are not well established, is the brevity of these bouts of sleep and wakefulness (1). In newborn rats at 2 days of age (P2), these cycles are astonishingly rapid: The average bout lengths of nuchal muscle atonia (indicative of sleep) and high nuchal muscle tone (indicative of wakefulness) are only 15 s and 5 s, respectively (2). Over the next week, bout lengths increase significantly as forebrain mechanisms exert increasing modulatory control over brainstem mechanisms controlling sleep and wakefulness (2).Recently, Lo et al. (3) analyzed the distributions of sleep and wake bouts in human adults. They found that, whereas sleep bouts exhibited an exponential distribution [such that the frequency distribution f(t) of bout durations of duration t was proportional to e (Ϫt/) , where is the characteristic time scale], wake bouts exhibited a power-law distribution [such that f(t) Ϸ t Ϫ␣ , where ␣ is a characteristic power-law exponent]. In a subsequent report (4), these findings were extended to cats, rats, and mice. From this comparative analysis, Lo and colleagues found that the exponential time scale for sleep bout durations increased with body size, thus possibly implicating a constitutional variable (e.g., metabolic rate) in the regulation of sleep bout...

The neurochemical changes underlying human emotions and social behavior are largely unknown. Here we report on the changes in the levels of two hypothalamic neuropeptides, hypocretin-1 (Hcrt-1) and melanin concentrating hormone (MCH), measured in the human amygdala. We show that Hcrt-1 levels are maximal during positive emotion, social interaction, and anger, behaviors that induce cataplexy in human narcoleptics. In contrast, MCH levels are minimal during social interaction, but are increased after eating. Both peptides are at minimal levels during periods of postoperative pain despite high levels of arousal. MCH levels increase at sleep onset, consistent with a role in sleep induction, whereas Hcrt-1 levels increase at wake onset, consistent with a role in wake induction. Levels of these two peptides in humans are not simply linked to arousal, but rather to specific emotions and state transitions. Other arousal systems may be similarly emotionally specialized.