Havekes Robbert, Abel Ted
Groningen Institute for Evolutionary Life Sciences (GELIFES), University of Groningen, Groningen, The Netherlands.
Iowa Neuroscience Institute and Department of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Curr Opin Neurobiol. 2017 Jun;44:13-19. doi: 10.1016/j.conb.2017.02.005. Epub 2017 Feb 27.
Memory consolidation, the process by which information is stored following training, consists of synaptic consolidation and systems consolidation. It is widely acknowledged that sleep deprivation has a profound effect on synaptic consolidation, particularly for memories that require the hippocampus. It is unclear, however, which of the many molecular changes associated with sleep deprivation directly contribute to memory deficits. In this review, we highlight recent studies showing that sleep deprivation impairs hippocampal cAMP and mTOR signaling, and ultimately causes spine loss in CA1 neurons in a cofilin-dependent fashion. Reversing these molecular alterations made memory consolidation resistant to the negative impact of sleep deprivation. Together, these studies have started to identify the molecular underpinnings by which sleep deprivation impairs synaptic consolidation.
记忆巩固是训练后信息存储的过程,包括突触巩固和系统巩固。人们普遍认为,睡眠剥夺对突触巩固有深远影响,尤其是对于需要海马体的记忆。然而,尚不清楚与睡眠剥夺相关的众多分子变化中,哪些直接导致记忆缺陷。在本综述中,我们重点介绍了最近的研究,这些研究表明睡眠剥夺会损害海马体中的环磷酸腺苷(cAMP)和雷帕霉素靶蛋白(mTOR)信号传导,并最终以一种依赖丝切蛋白的方式导致CA1神经元中的树突棘丢失。逆转这些分子改变可使记忆巩固对睡眠剥夺的负面影响产生抗性。总之,这些研究已开始确定睡眠剥夺损害突触巩固的分子基础。