Nishida Masaki, Nakashima Yusaku, Nishikawa Toru
Department of Psychiatry and Behavioral Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima, Bunkyo, Japan.
Medical Technology Research Laboratory, Research and Development Division, Medical Business Unit, Sony Corporation, Tokyo, Japan.
Nat Sci Sleep. 2016 Jan 28;8:63-72. doi: 10.2147/NSS.S100337. eCollection 2016.
Evidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process.
Healthy control participants (n=17) and patients medicated for major depressive disorder (n=11) were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand) paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement). Participants' brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs). Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5-16 Hz) and slow-frequency spindle activity (10.5-12.5 Hz).
Sleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups.
Because the changes in slow-frequency spindle activity affected the thalamocortical network dysfunction in patients medicated for depression, dysregulated spindle generation may impair sleep-dependent memory consolidation. Our findings may help to elucidate the cognitive deficits that occur in patients with major depression both in the waking state and during sleep.
已有证据表明，在健康个体中，睡眠可增强程序性记忆巩固，且睡眠纺锤波活动调节这一过程。然而，服用抗重度抑郁症药物的患者是否存在依赖睡眠的程序性记忆巩固尚不清楚，这一过程背后的药理和生理机制也不明确。
招募健康对照参与者（n = 17）和服用抗重度抑郁症药物的患者（n = 11），让他们接受手指敲击运动序列测试（MST；非优势手）范式，以比较不同学习阶段（睡前、睡后和夜间改善）的平均得分。在睡眠期间通过16个脑电图通道记录参与者的大脑活动（在MST之间）。对脑电图数据进行睡眠评分和频率分析。此外，我们评估了睡眠纺锤波活动，将纺锤波分为快频率纺锤波活动（12.5 - 16赫兹）和慢频率纺锤波活动（10.5 - 12.5赫兹）。
与对照参与者相比，抑郁症患者依赖睡眠的运动记忆巩固受损。在抑郁症患者中，年龄与夜间改善呈负相关。慢波睡眠时长与抑郁症患者的运动记忆巩固程度相关，而在健康对照中则不然。慢频率纺锤波活动与两组的运动记忆巩固程度降低有关。
由于慢频率纺锤波活动的变化影响了服用抗抑郁药物患者的丘脑皮质网络功能障碍，纺锤波生成失调可能会损害依赖睡眠的记忆巩固。我们的研究结果可能有助于阐明重度抑郁症患者在清醒状态和睡眠期间出现的认知缺陷。
