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Abstract
Sleep affects brain activity globally, but many cortical sleep waves are spatially confined. Local rhythms serve cortical area-specific sleep needs and functions; however, mechanisms controlling locality are unclear. We identify the thalamic reticular nucleus (TRN) as a source for local, sensory-cortex-specific non-rapid-eye-movement sleep (NREMS) in mouse. Neurons in optogenetically identified sensory TRN sectors showed stronger repetitive burst discharge compared to non-sensory TRN cells due to higher activity of the low-threshold Ca2+ channel CaV3.3. Major NREMS rhythms in sensory but not non-sensory cortical areas were regulated in a CaV3.3-dependent manner. In particular, NREMS in somatosensory cortex was enriched in fast spindles, but switched to delta wave-dominated sleep when CaV3.3 channels were genetically eliminated or somatosensory TRN cells chemogenetically hyperpolarized. Our data indicate a previously unrecognized heterogeneity in a powerful forebrain oscillator that contributes to sensory-cortex-specific and dually regulated NREMS, enabling local sleep regulation according to use- and experience-dependence.
Highlights
Sleep is a global vigilance state with well-known behavioral, electroencephalographic and neuromodulatory attributes
It arises through heterogeneity in thalamic circuits and correlates with variable oscillatory bursting propensity across thalamic reticular nucleus (TRN) sectors
Strong CaV3.3-dependent bursting in the somatosensory TRN sector led to local non-rapid-eye-movement sleep (NREMS) with fast and large spindles coupled to the SO, whereas this was not the case for cortical areas corresponding to TRN sectors with weakly bursting cells
Summary
Sleep is a global vigilance state with well-known behavioral, electroencephalographic and neuromodulatory attributes. Cerebral correlates of non-rapid-eye-movement sleep (NREMS) and REMS, notably several major EEG sleep rhythms, occur variably at different times in different brain regions (Massimini et al, 2004; Nir et al, 2011; Siclari and Tononi, 2017). This suggests that, on top of a global regulation, forebrain pacemakers with regionally specific oscillatory properties shape sleep across the cortex (Krueger et al, 2013). Sleep disorders may arise from a pathologically altered spatial heterogeneity that negatively impacts sleep as a global state (Krueger et al, 2013; Siclari and Tononi, 2017)
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