Abstract
Sleep is thought to be involved in the regulation of synaptic plasticity in two ways: by enhancing local plastic processes underlying the consolidation of specific memories and by supporting global synaptic homeostasis. Here, we briefly summarize recent structural and functional studies examining sleep-associated changes in synaptic morphology and neural excitability. These studies point to a global down-scaling of synaptic strength across sleep while a subset of synapses increases in strength. Similarly, neuronal excitability on average decreases across sleep, whereas subsets of neurons increase firing rates across sleep. Whether synapse formation and excitability is down or upregulated across sleep appears to partly depend on the cell’s activity level during wakefulness. Processes of memory-specific upregulation of synapse formation and excitability are observed during slow wave sleep (SWS), whereas global downregulation resulting in elimination of synapses and decreased neural firing is linked to rapid eye movement sleep (REM sleep). Studies of the excitation/inhibition balance in cortical circuits suggest that both processes are connected to a specific inhibitory regulation of cortical principal neurons, characterized by an enhanced perisomatic inhibition via parvalbumin positive (PV+) cells, together with a release from dendritic inhibition by somatostatin positive (SOM+) cells. Such shift towards increased perisomatic inhibition of principal cells appears to be a general motif which underlies the plastic synaptic changes observed during sleep, regardless of whether towards up or downregulation.
Highlights
Research of the last decades has identified sleep as a key contributor to the continuing changes the brain undergoes while adapting to its environment
By comparing averaged Ca2+ activity during wakefulness, slow wave sleep (SWS) and rapid eye movement (REM) sleep epochs, in a first study (Niethard et al, 2016), we found that both sleep stages were accompanied by a distinct decrease in Pyr cell activity relative to wakefulness; during SWS, such decrease was paralleled by reduced PV+ and SOM+ cell activity (Niethard et al, 2016; Figure 2)
Sleep serves a dual function in regulating cortical network plasticity, i.e., to locally strengthen circuits that represent freshly encoded memories, and to globally re-normalize synaptic connectivity according to homeostatic principles
Summary
Research of the last decades has identified sleep as a key contributor to the continuing changes the brain undergoes while adapting to its environment. Monitoring of task-related synaptic networks provided the first indications that the memory-specific up-scaling of synapses in dendritic branches of layer 5 pyramidal neurons occurs during SWS, whereas the elimination of newly formed spines in branches not undergoing task-specific reactivation is supported by REM sleep.
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