Person:

Nunn, Charles

Background: All animals thus far studied sleep, but little is known about the ecological factors that generate differences in sleep characteristics across species, such as total sleep duration or division of sleep into multiple bouts across the 24-hour period (i.e., monophasic or polyphasic sleep activity). Here we address these questions using an evolutionary agent-based model. The model is spatially explicit, with food and sleep sites distributed in two clusters on the landscape. Agents acquire food and sleep energy based on an internal circadian clock coded by 24 traits (one for each hour of the day) that correspond to "genes" that evolve by means of a genetic algorithm. These traits can assume three different values that specify the agents' behavior: sleep (or search for a sleep site), eat (or search for a food site), or flexibly decide action based on relative levels of sleep energy and food energy. Individuals with higher fitness scores leave more offspring in the next generation of the simulation, and the model can therefore be used to identify evolutionarily adaptive circadian clock parameters under different ecological conditions. Results: We systematically varied input parameters related to the number of food and sleep sites, the degree to which food and sleep sites overlap, and the rate at which food patches were depleted. Our results reveal that: (1) the increased costs of traveling between more spatially separated food and sleep clusters select for monophasic sleep, (2) more rapid food patch depletion reduces sleep times, and (3) agents spend more time attempting to acquire the "rarer" resource, that is, the average time spent sleeping is positively correlated with the number of food patches and negatively correlated with the number of sleep patches. "Flexible" genes, in general, do not appear to be advantageous, though their arrangements in the agents' genome show characteristic patterns that suggest that selection acts on their distribution. Conclusion: Collectively, the output suggests that ecological factors can have striking effects on sleep patterns. Moreover, our results demonstrate that a simple model can produce clear and sensible patterns, thus allowing it to be used to investigate a wide range of questions concerning the ecology of sleep. Quantitative data presently are unavailable to test the model predictions directly, but patterns are consistent with comparative evidence from different species, and the model can be used to target ecological factors to investigate in future research.

Sleep is a pervasive characteristic of mammalian species, yet its purpose remains obscure. It is often proposed that ‘sleep is for the brain’, a view that is supported by experimental studies showing that sleep improves cognitive processes such as memory consolidation. Some comparative studies have also reported that mammalian sleep durations are higher among more encephalized species. However, no study has assessed the relationship between sleep and the brain structures that are implicated in specific cognitive processes across species. The hippocampus, neocortex and amygdala are important for memory consolidation and learning and are also in a highly actived state during sleep. We therefore investigated the evolutionary relationship between mammalian sleep and the size of these brain structures using phylogenetic comparative methods. We found that evolutionary increases in the size of the amygdala are associated with corresponding increases in NREM sleep durations. These results are consistent with the hypothesis that NREM sleep is functionally linked with specializations of the amygdala, including perhaps memory processing.

Background: Sleep is a biological enigma. Despite occupying much of an animal's life, and having been scrutinized by numerous experimental studies, there is still no consensus on its function. Similarly, no hypothesis has yet explained why species have evolved such marked variation in their sleep requirements (from 3 to 20 hours a day in mammals). One intriguing but untested idea is that sleep has evolved by playing an important role in protecting animals from parasitic infection. This theory stems, in part, from clinical observations of intimate physiological links between sleep and the immune system. Here, we test this hypothesis by conducting comparative analyses of mammalian sleep, immune system parameters, and parasitism. Results: We found that evolutionary increases in mammalian sleep durations are strongly associated with an enhancement of immune defences as measured by the number of immune cells circulating in peripheral blood. This appeared to be a generalized relationship that could be independently detected in 4 of the 5 immune cell types and in both of the main sleep phases. Importantly, no comparable relationships occur in related physiological systems that do not serve an immune function. Consistent with an influence of sleep on immune investment, mammalian species that sleep for longer periods also had substantially reduced levels of parasitic infection. Conclusion: These relationships suggest that parasite resistance has played an important role in the evolution of mammalian sleep. Species that have evolved longer sleep durations appear to be able to increase investment in their immune systems and be better protected from parasites. These results are neither predicted nor explained by conventional theories of sleep evolution, and suggest that sleep has a much wider role in disease resistance than is currently appreciated.