Abstract: Healthy sleep is implicated in cognitive functioning, especially sleep-dependent memory consolidation (SDC). Insomnia, a common sleep disorder mainly characterized by sleep disturbances, has become a prominent problem in modern society. Its impact on SDC has also attracted increased attention. Therefore, this paper aimed to review previous studies on the effects of primary insomnia (PI) on SDC of different types of memory, and to elucidate the neural mechanism of SDC changes in PI, so as to provide theoretical support for improving the SDC of PI patients. According to previous studies, the influence of PI on SDC mainly focused on declarative memory (semantic memory) and non-declarative memory (procedural memory), and the conclusions seem to be inconsistent. Generally speaking, SDC of procedural memory was found to be more susceptible to PI, while the influence of PI on SDC of declarative memory was relatively mild. Most existing studies found that PI patients had greater impairment in procedural memory consolidation than healthy sleepers. However, only one study showed that SDC of declarative memory in patients with PI was defective. Moreover, SDC of declarative memory in patients with PI was more vulnerable to interference learning than that of procedural memory. The differences in experimental design, SDC paradigm type, first-night effect, sample characteristics, and sleep structure may be the reasons for this inconsistency. To date, the mechanisms of the effects of PI on the SDC of declarative and procedural memories are still unclear. Some polysomnographic studies have demonstrated that the influence of PI on SDC is linked to certain macrostructures and microstructures of sleep. Specifically, a previous study showed that the amount of slow wave sleep (SWS) decreased significantly in PI patients, and the compensatory increase in rapid eye movement sleep (REM) had a positive correlation with SDC of declarative memory in patients. In another study, PI patients had a diminished amount of REM, but there was no correlation between SDC impairments of procedural memory and REM in the PI group. Furthermore, no SWS compensation was observed in patients, indicating that REM may play an irreplaceable role in SDC of procedural memory. In addition, the damage of different functional brain regions in insomnia patients may hinder SDC of declarative or procedural memory, which is mainly due to the relationships between SDC of different memory types and different brain structures. However, there is no direct evidence to support this hypothesis. Overall, based on the disruption of sleep structure and abnormal brain structures in insomnia patients and the relationships between these changes and SDC in PI, it can be speculated that the effect of PI on SDC of declarative and procedural memories could be consistent with the system consolidation hypothesis and synaptic homeostasis hypothesis. In essence, the potential brain mechanisms of PI on SDC are dependent on system consolidation and synaptic consolidation. Future studies could be conducted on the synchronous acquisition of behavioral, electroencephalographic, and brain imaging data to explore the neural pathways of SDC associated with insomnia, and on the prevention and treatment of SDC impairment in patients with PI through transcranial current stimulation, transcranial magnetic stimulation, or targeted memory reactivation.

Key words: primary insomnia, sleep-dependent memory consolidation, declarative memory, procedural memory, system consolidation hypothesis, synaptic homeostasis hypothesis

摘要： 现代社会的失眠问题异常突出，其对睡眠依赖性记忆巩固（SDC）的影响日益引起重视。目前，原发性失眠（PI）对陈述性及程序性记忆SDC的影响存在分歧。梳理以往研究发现，系统巩固假说和突触稳态假说支持睡眠结构紊乱及脑结构异常可能是PI患者SDC损伤的潜在脑机制。未来研究可考虑同步采集行为、脑电和脑成像数据，深入探究PI影响SDC的脑机制，并验证上述假说；还可尝试通过经颅电/磁刺激和目标记忆重激活等无创性干预措施改善PI患者的SDC效应。

关键词: 原发性失眠, 睡眠依赖性记忆巩固, 陈述性记忆, 程序性记忆, 系统巩固假说, 突触稳态假说