Simor Attila, Györffy Balázs András, Gulyássy Péter, Völgyi Katalin, Tóth Vilmos, Todorov Mihail Ivilinov, Kis Viktor, Borhegyi Zsolt, Szabó Zoltán, Janáky Tamás, Drahos László, Juhász Gábor, Kékesi Katalin Adrienna
Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Budapest H-1117, Hungary.
Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Budapest H-1117, Hungary; MTA-ELTE NAP B Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, Eötvös Loránd University, Budapest H-1117, Hungary.
Mol Cell Neurosci. 2017 Mar;79:64-80. doi: 10.1016/j.mcn.2017.01.002. Epub 2017 Jan 10.
Acute total sleep deprivation (SD) impairs memory consolidation, attention, working memory and perception. Structural, electrophysiological and molecular experimental approaches provided evidences for the involvement of sleep in synaptic functions. Despite the wide scientific interest on the effects of sleep on the synapse, there is a lack of systematic investigation of sleep-related changes in the synaptic proteome. We isolated parietal cortical and thalamic synaptosomes of rats after 8h of total SD by gentle handling and 16h after the end of deprivation to investigate the short- and longer-term effects of SD on the synaptic proteome, respectively. The SD efficiency was verified by electrophysiology. Protein abundance alterations of the synaptosomes were analyzed by fluorescent two-dimensional differential gel electrophoresis and by tandem mass spectrometry. As several altered proteins were found to be involved in synaptic strength regulation, our data can support the synaptic homeostasis hypothesis function of sleep and highlight the long-term influence of SD after the recovery sleep period, mostly on cortical synapses. Furthermore, the large-scale and brain area-specific protein network change in the synapses may support both ideas of sleep-related synaptogenesis and molecular maintenance and reorganization in normal rat brain.
急性完全睡眠剥夺(SD)会损害记忆巩固、注意力、工作记忆和感知能力。结构、电生理和分子实验方法为睡眠参与突触功能提供了证据。尽管睡眠对突触的影响引起了广泛的科学关注,但对于突触蛋白质组中与睡眠相关的变化缺乏系统研究。我们通过轻柔处理,在大鼠完全睡眠剥夺8小时后分离其顶叶皮质和丘脑突触体,并在剥夺结束后16小时分离,分别研究睡眠剥夺对突触蛋白质组的短期和长期影响。通过电生理学验证睡眠剥夺效率。通过荧光二维差异凝胶电泳和串联质谱分析突触体的蛋白质丰度变化。由于发现几种改变的蛋白质参与突触强度调节,我们的数据可以支持睡眠的突触稳态假说功能,并突出恢复睡眠期后睡眠剥夺的长期影响,主要是对皮质突触的影响。此外,突触中大规模且特定脑区的蛋白质网络变化可能支持正常大鼠大脑中与睡眠相关的突触形成以及分子维持和重组的观点。