<p>Sleep disturbances frequently occur in depression, stemming from the pathophysiology of the disorder and its pharmacological treatment. Antidepressants exert intricate, class-specific effects on sleep architecture, influencing rapid eye movement (REM) latency and density, slow-wave sleep, and overall sleep quality. Although some of these changes might contribute to the therapeutic efficacy, they can also worsen sleep problems and cause daytime fatigue. Recent findings suggest that alterations in REM sleep may serve as potential indicators of antidepressant response, particularly for drugs that strongly affect sleep architecture. Among antidepressants, selective serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors most consistently suppress REM sleep and fragment sleep continuity, whereas drugs with receptor-modulating or melatonergic properties, such as agomelatine or mirtazapine, tend to preserve restorative sleep stages and improve circadian alignment. Understanding how antidepressants influence sleep structure and related neurobiological mechanisms is essential for optimizing treatment strategies. Enhancing sleep quality may not only potentiate the therapeutic effects of antidepressants but also contribute to overall patient outcomes. Implementing standardized sleep assessment methods would facilitate research on the effects of long-term antidepressant treatment and help clinicians tailor treatments based on antidepressant efficacy, sleep-related impact, and patient-specific symptoms.</p>