<p>Sleep disturbances are among the most prevalent and early-emerging features of autism spectrum disorder (ASD), often preceding core behavioral symptoms. Despite their clinical relevance, the neurobiological mechanisms driving early-life sleep disruption in ASD remain poorly understood. <i>Shank3</i>, encoding a synaptic scaffolding protein at excitatory synapses, is one of the most well-established monogenic risk factors for ASD. Here, we systematically investigated sleep architecture and homeostatic regulation in juvenile <i>Shank3</i>^Δe11–21 rats, which lack Shank3 protein and display ASD-like behavioral and sensory phenotypes. EEG/EMG recordings revealed sex-specific abnormalities: males exhibited fragmented sleep with frequent brief arousals, whereas females showed prolonged wakefulness. Both sexes demonstrated reduced NREM sleep δ power, indicating diminished sleep depth. Following 6-h sleep deprivation, <i>Shank3</i>^−/− rats displayed blunted homeostatic rebound. Additionally, <i>Clock</i> and <i>Bmal1</i> mRNA were significantly downregulated in prefrontal cortex and striatum, implicating circadian dysregulation within corticostriatal circuits. Collectively, these findings indicate that <i>Shank3</i> deficiency leads to early-onset, low-quality sleep accompanied by impaired homeostatic and circadian regulation. This phenotype mirrors clinical sleep disturbances in children with ASD, supporting sleep dysfunction as an intrinsic, early feature of <i>Shank3</i>-related pathophysiology. Together with prior behavioral evidence, this study establishes the <i>Shank3</i>^Δe11–21 rat as a preclinical model for elucidating mechanisms of <i>Shank3</i>-related neurodevelopmental disorders and for evaluating potential early-life therapeutic interventions, including sleep-targeted strategies.</p><p></p>