Reactivation in cortical and subcortical systems during consolidation of declarative memory - investigations in wakefulness and sleep

编码后，新的记忆痕迹最初是脆弱的，必须经历一个巩固的过程。这些过程可以发生在突触水平以及系统水平上。睡眠已被证明对几种类型的记忆起着重要作用。最有影响力的理论之一指出，在睡眠期间，新的记忆痕迹被反复激活，从而在不同的存储位置之间进行强化，再加工和转移。本研究从这一假设出发，探讨人类陈述性记忆中记忆巩固的脑机制。基于以前的研究，将特别关注睡眠期间发生的一些协调事件：睡眠慢振荡，睡眠纺锤波，海马和蓝斑（LC）活动。使用一个新的任务，可以更有效地研究睡眠对记忆的影响，学习和回忆之间的干扰影响的问题将得到解决。EEG研究计划在强化学习后的睡眠期间发现持续的大脑活动中记忆重新激活的迹象。结合脑电图/功能磁共振成像将被用来测试目前的假设，记忆转移之间的不同大脑区域在睡眠中。通过去甲肾上腺素能系统的药理学操作和同步功能性磁共振成像（fMRI），LC对记忆巩固的贡献将被研究。此外，将检查降低去甲肾上腺素能活性的药物对长期记忆功能的影响。

After encoding, new memory traces are initially fragile and have to undergo a process of consolidation. These processes can occur at the synaptic level as well as on a systems level. Sleep has been shown to play an important role for several types of memory. One of the most influential theories states that during sleep, new memory traces are reactivated repeatedly and thus strengthened, reprocessed and transferred between different storage locations. Starting from this hypothesis, the present project aims to find brain mechanisms which underlie memory consolidation in human declarative memory. Based on previous studies, special attention will be given to a number of coordinated events occurring during sleep: the sleep slow oscillation, sleep spindles, hippocampal and locus coeruleus (LC) activity. Using a new task that allows to study the effect of sleep on memory more efficiently, questions of the influence of interference intervening between learning and recall will be addressed. EEG studies are planned to find signs of memory reactivation in ongoing brain activity during sleep after periods of intensive learning. Combined EEG/fMRI will be used to test current hypothesis of memory transfer between different brain regions during sleep. By means of pharmacological manipulation of the noradrenergic system and concurrent functional magnetic resonance imaging (fMRI), the contribution of the LC to memory consolidation will be investigated. Additionally, the impact of medications reducing noradrenergic activity on long‐term memory function will be examined.