Sharpley A L, Cowen P J
Oxford University, Department of Psychiatry, Littlemore, United Kingdom.
Biol Psychiatry. 1995 Jan 15;37(2):85-98. doi: 10.1016/0006-3223(94)00135-P.
Antidepressant drugs produce striking effects on sleep architecture that are best understood in terms of their interactions with the monoamine pathways controlling sleep and wakefulness. Many different antidepressant drugs, including tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and selective 5-hydroxytryptamine (5-HT; serotonin) reuptake inhibitors (SSRIs), decrease rapid eye movement (REM) sleep. The reduction in REM sleep produced by antidepressants may be an important part of their mechanism of action; however, the ability of new antidepressant compounds, such as nefazodone and moclobemide, to increase REM sleep throws doubt on this suggestion. The effects of antidepressants on slow-wave sleep (SWS) are quite diverse; in general, antidepressants having significant 5-HT2A/2C receptor antagonist properties increase SWS, whereas other drugs, such as SSRIs or MAOIs, either lower SWS or produce no change. Sleep continuity is improved acutely following administration of antidepressants with sedating properties such as certain TCAs, trazodone, and mianserin. Some nonsedating drugs (ritanserin and nefazodone) also improve sleep continuity measures, possibly through 5-HT2A/2C receptor blockade.
抗抑郁药物对睡眠结构产生显著影响，若从它们与控制睡眠和觉醒的单胺通路的相互作用方面来理解，这些影响最为清晰。许多不同的抗抑郁药物，包括三环类抗抑郁药（TCAs）、单胺氧化酶抑制剂（MAOIs）和选择性5-羟色胺（5-HT；血清素）再摄取抑制剂（SSRIs），都会减少快速眼动（REM）睡眠。抗抑郁药物引起的REM睡眠减少可能是其作用机制的重要组成部分；然而，新型抗抑郁化合物，如奈法唑酮和吗氯贝胺，能够增加REM睡眠，这对此观点提出了质疑。抗抑郁药物对慢波睡眠（SWS）的影响相当多样；一般来说，具有显著5-HT2A/2C受体拮抗剂特性的抗抑郁药物会增加SWS，而其他药物，如SSRIs或MAOIs，则会降低SWS或不产生变化。服用具有镇静特性的抗抑郁药物，如某些TCAs、曲唑酮和米安色林后，睡眠连续性会迅速改善。一些非镇静药物（利坦色林和奈法唑酮）也能改善睡眠连续性指标，可能是通过阻断5-HT2A/2C受体实现的。
