Academic journal article Genetics

Sleep and Development in Genetically Tractable Model Organisms

Academic journal article Genetics

Sleep and Development in Genetically Tractable Model Organisms

Article excerpt

DISORDERS disrupting sleep during childhood and adolescence undermine physical health as well as emotional, cognitive, and social development. Therefore, despite caveats associated with any single line of evidence, sleep is widely believed to play a crucial role in the developing brain (Owens 2014). Despite great interest and progress, the interplay between sleep and development is not well understood. In their seminal article, Roffwarg et al. (1966) demonstrated in humans that the total amount of daily sleep and the percentage of rapid eye movement (REM) sleep peak in infancy and decrease with age (Kleitman and Engelmann 1953; Parmelee et al. 1961; Roffwarg et al. 1966; Hoppenbrouwers and Sterman 1975; Awoust and Levi 1984). This maturation of sleep characteristics as an organism develops from embryo to mature adult is referred to as sleep ontogeny or ontogenetic sleep changes. Similar trends, where the amount of total sleep, or vertebrate REM sleep, is highest early in development, have been observed inmammals, fish, birds, insects, and nematodes (Jouvet-Mounier et al. 1970; McGinty et al. 1977; Szymczak 1987; Shaw et al. 2000; Kirov and Moyanova 2002; Paredes et al. 2006; Raizen et al. 2008; Hasan et al. 2012; Todd et al. 2012; Sorribes 2013). These findings led to the hypothesis that during early life, REM sleep and invertebrate sleep may play an important role in the development of the nervous system, by establishing a period of globally heightened plasticity and/ or providing endogenous, specialized activity in certain neural circuits (O'Donovan 1999; Mohns and Blumberg 2008, 2010; Blumberg et al. 2013; Corner 2013). Such specialized activity could, for instance, promote appropriate neurodevelopment through feedback by coupling function (such as recurring limb movement) to the refinement of neural connections. Consistent with this notion, nonlethal deprivation can cause longlasting neurological and behavioral defects in vertebrates and invertebrates alike (Halbower et al. 2006; Jan et al. 2010; Kayser et al. 2014). Yet a mechanistic grasp is lacking with regard to how sleep ontogeny is controlled and why inadequate sleep during development is particularly deleterious.

How can relatively simple models inform such broad questions? The universality of sleep in the animal kingdom has been a matter of long-standing debate, but it is now widely accepted that zebrafish, fruit flies, and nematodes sleep (Table 1; Cirelli and Tononi 2008). As discussed below, sleep is developmentally regulated across these species, suggesting deep conservation of ontogenetic sleep changes and providing an opportunity to leverage the powerful genetic approaches in these systems to answer questions at the intersection of sleep and development. Here, we review the connections between sleep and appropriate development of nervous systems with a focus on genetic model organisms. Recent findings in fish, flies, and nematodes join and expand on studies of mammalian sleep in immature states. Taken together, this work suggests a fundamental role for sleep in patterning of the brain and sculpting neural circuits throughout development.

Negative Impacts of Disrupted Sleep During Mammalian Development

One of the strongest pieces of evidence to suggest a privileged role for sleep during development is the unique consequence of disturbed sleep within this period. Testing this idea has proved difficult in humans and other mammals. Most work in humans has taken advantage of a common and naturally occurring sleep disruptor, obstructive sleep apnea (OSA). OSA in adults and children alike results in numerous complications, including cognitive dysfunction (Findley et al. 1986; Gozal 1998; Beebe et al. 2003; Archbold et al. 2004). Indeed in children, sleep-disordered breathing has been associated with reduced cognitive function and general intelligence, as well as neuroimaging-based evidence for prefrontal cortical abnormalities (Schechter 2002; Gottlieb et al. …

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