Sleep disturbances are an integral part of depressive disorder. As such, they are a part of all contemporary sets of diagnostic criteria for major depression and of all major symptom-based rating scales for depression. Insomnia is a particularly frequent complaint, and it is reported by more than 90% of depressed patients. Although the "kindling" or "illness transduction" model of depression remains hypothetical, there is evidence that people with recurrent depression have more pronounced abnormalities of sleep neurophysiology than those experiencing a single or initial episode. Therefore, early relief of insomnia in a depressed patient, in addition to alleviating other symptoms, may increase adherence to treatment and increase daytime performance and overall functioning, while complete relief of insomnia may improve prognosis. Stimulation of serotonin-2 (5-HT2) receptors is thought to underlie insomnia and changes in sleep architecture seen with selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs). This is the reason why hypnotics or low-dose trazodone are commonly coprescribed at the initiation of the treatment with either the SSRIs or SNRIs. On the other hand, antidepressant drugs with 5-HT2 blocking properties, such as mirtazapine or nefazodone, alleviate insomnia and improve sleep architecture. In depressed patients, mirtazapine produces a significant shortening of sleep-onset latency, increases a total sleep time, and leads to a marked improvement in sleep efficiency. Antidepressants with preferential 5-HT2 blocking properties are therefore a good treatment option for depressed patients with marked insomnia.