Plasticity during Sleep Is Linked to Specific Regulation of Cortical Circuit Activity. Niethard Niels,Burgalossi Andrea,Born Jan Frontiers in neural circuits 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. 10.3389/fncir.2017.00065

Striatal adenosine A receptor neurons control active-period sleep via parvalbumin neurons in external globus pallidus. Yuan Xiang-Shan,Wang Lu,Dong Hui,Qu Wei-Min,Yang Su-Rong,Cherasse Yoan,Lazarus Michael,Schiffmann Serge N,d'Exaerde Alban de Kerchove,Li Rui-Xi,Huang Zhi-Li eLife Dysfunction of the striatum is frequently associated with sleep disturbances. However, its role in sleep-wake regulation has been paid little attention even though the striatum densely expresses adenosine A receptors (ARs), which are essential for adenosine-induced sleep. Here we showed that chemogenetic activation of AR neurons in specific subregions of the striatum induced a remarkable increase in non-rapid eye movement (NREM) sleep. Anatomical mapping and immunoelectron microscopy revealed that striatal AR neurons innervated the external globus pallidus (GPe) in a topographically organized manner and preferentially formed inhibitory synapses with GPe parvalbumin (PV) neurons. Moreover, lesions of GPe PV neurons abolished the sleep-promoting effect of striatal AR neurons. In addition, chemogenetic inhibition of striatal AR neurons led to a significant decrease of NREM sleep at active period, but not inactive period of mice. These findings reveal a prominent contribution of striatal AR neuron/GPe PV neuron circuit in sleep control. 10.7554/eLife.29055

Hippocampal Network Oscillations Rescue Memory Consolidation Deficits Caused by Sleep Loss. Ognjanovski Nicolette,Broussard Christopher,Zochowski Michal,Aton Sara J Cerebral cortex (New York, N.Y. : 1991) Oscillations in the hippocampal network during sleep are proposed to play a role in memory storage by patterning neuronal ensemble activity. Here we show that following single-trial fear learning, sleep deprivation (which impairs memory consolidation) disrupts coherent firing rhythms in hippocampal area CA1. State-targeted optogenetic inhibition of CA1 parvalbumin-expressing (PV+) interneurons during postlearning NREM sleep, but not REM sleep or wake, disrupts contextual fear memory (CFM) consolidation in a manner similar to sleep deprivation. NREM-targeted inhibition disrupts CA1 network oscillations which predict successful memory storage. Rhythmic optogenetic activation of PV+ interneurons following learning generates CA1 oscillations with coherent principal neuron firing. This patterning of CA1 activity rescues CFM consolidation in sleep-deprived mice. Critically, behavioral and optogenetic manipulations that disrupt CFM also disrupt learning-induced stabilization of CA1 ensembles' communication patterns in the hours following learning. Conversely, manipulations that promote CFM also promote long-term stability of CA1 communication patterns. We conclude that sleep promotes memory consolidation by generating coherent rhythms of CA1 network activity, which provide consistent communication patterns within neuronal ensembles. Most importantly, we show that this rhythmic patterning of activity is sufficient to promote long-term memory storage in the absence of sleep. 10.1093/cercor/bhy174

Thalamic Drive of Cortical Parvalbumin-Positive Interneurons during Down States in Anesthetized Mice. Current biology : CB Up and down states are among the most prominent features of the thalamo-cortical system during non-rapid eye movement (NREM) sleep and many forms of anesthesia. Cortical interneurons, including parvalbumin (PV) cells, display firing activity during cortical down states, and this GABAergic signaling is associated with prolonged down-state durations. However, what drives PV interneurons to fire during down states remains unclear. We here tested the hypothesis that background thalamic activity may lead to suprathreshold activation of PV cells during down states. To this aim, we performed two-photon guided juxtasomal recordings from PV interneurons in the barrel field of the somatosensory cortex (S1bf) of anesthetized mice, while simultaneously collecting the local field potential (LFP) in S1bf and the multi-unit activity (MUA) in the ventral posteromedial (VPM) thalamic nucleus. We found that activity in the VPM was associated with longer down-state duration in S1bf and that down states displaying PV cell firing were associated with increased VPM activity. Moreover, thalamic inhibition through application of muscimol reduced the fraction of spikes discharged by PV cells during cortical down states. Finally, we inhibited PV interneurons using optogenetics during down states while monitoring cortical LFP under control conditions and after thalamic muscimol injection. We found increased latency of the optogenetically triggered down-to-up transitions upon thalamic pharmacological blockade compared to controls. These findings demonstrate that spontaneous thalamic activity inhibits cortex during down states through the activation of PV interneurons. 10.1016/j.cub.2019.04.007