Brain Institute, Federal University of Rio Grande do Norte (UFRN), Natal, Rio Grande do Norte, Brazil.
Pflugers Arch. 2012 Jan;463(1):111-20. doi: 10.1007/s00424-011-1031-5. Epub 2011 Sep 27.
While there is ample agreement that the cognitive role of sleep is explained by sleep-dependent synaptic changes, consensus is yet to be established as to the nature of these changes. Some researchers believe that sleep promotes global synaptic downscaling, leading to a non-Hebbian reset of synaptic weights that is putatively necessary for the acquisition of new memories during ensuing waking. Other investigators propose that sleep also triggers experience-dependent, Hebbian synaptic upscaling able to consolidate recently acquired memories. Here, I review the molecular and physiological evidence supporting these views, with an emphasis on the calcium signaling pathway. I argue that the available data are consistent with sleep promoting experience-dependent synaptic embossing, understood as the simultaneous non-Hebbian downscaling and Hebbian upscaling of separate but complementary sets of synapses, heterogeneously activated at the time of memory encoding and therefore differentially affected by sleep.
虽然人们普遍认为睡眠对认知的作用是通过睡眠依赖的突触变化来解释的，但对于这些变化的性质还没有达成共识。一些研究人员认为，睡眠促进了全局突触缩小，导致了突触权重的非赫布式重置，这被认为是在随后的清醒期间获得新记忆所必需的。其他研究人员则提出，睡眠还会触发依赖经验的赫布式突触放大，从而巩固最近获得的记忆。在这里，我回顾了支持这些观点的分子和生理学证据，重点是钙信号通路。我认为，现有数据与睡眠促进经验依赖性突触压痕是一致的，这种压痕被理解为同时进行的非赫布式和赫布式的分离但互补的突触子集的缩小和放大，这些突触子集在记忆编码时是异质激活的，因此受到睡眠的不同影响。
