| Summary: | Sleep abnormalities are common in patients with neurodevelopmental disorders, and it is thought that deficits in sleep may contribute to the unfolding of symptoms in these disorders. Appreciating sleep abnormalities in neurodevelopmental disorders could be important for designing a treatment for these disorders. We studied sleep duration in three mouse models by means of home-cage monitoring: <i>Tsc2</i><sup>+/−</sup> (tuberous sclerosis complex), oxytocin receptor (<i>Oxtr</i>) knockout (KO) (autism spectrum disorders), and <i>Shank3 <sup>e4-9</sup></i> KO (Phelan–McDermid syndrome). We studied both male and female mice, and data were analyzed to examine effects of both genotype and sex. In general, we found that female mice slept less than males regardless of genotype or phase. We did not find any differences in sleep duration in either <i>Tsc2</i><sup>+/−</sup> or <i>Oxtr</i> KO mice, compared to controls. In <i>Shank3 <sup>e4-9</sup></i> KO mice, we found a statistically significant genotype x phase interaction (<i>p</i> = 0.002) with a trend that <i>Shank3</i><i><sup>e4-9</sup></i> KO mice regardless of sex slept more than control mice in the active phase. Our results have implications for the management of patients with Phelan–McDermid syndrome.
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