Thalamic reticular control of local sleep in mouse sensory cortex.
basic_science · Level V
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- Record sourced from PubMed, PMID 30583750.
- Also identified by DOI 10.7554/eLife.39111 and PMC identifier 6342525.
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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 Ca<sup>2+</sup> channel Ca<sub>V</sub>3.3. Major NREMS rhythms in sensory but not non-sensory cortical areas were regulated in a Ca<sub>V</sub>3.3-dependent manner. In particular, NREMS in somatosensory cortex was enriched in fast spindles, but switched to delta wave-dominated sleep when Ca<sub>V</sub>3.3 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.
Medical subject headings
- Sleep
- Somatosensory Cortex
- Thalamic Nuclei