Journal
NATURE NEUROSCIENCE
Volume 19, Issue 2, Pages 290-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4209
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Funding
- Strauss Clinical Fellowship
- Human Frontier Science Program [RGY0076/2012]
- Douglas Foundation
- McGill University
- Canadian Fund for Innovation (CFI)
- Canadian Research Chair (CRC Tier 2)
- Canadian Institute for Health Research (CIHR)
- Natural Science and Engineering Council of Canada (NSERC)
- Inselspital
- Swiss National Fund
- University of Bern
- Deutsche Forschungsgemeinschaft (DFG) [Exc 257 NeuroCure, SPP1665]
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During non-rapid eye movement (NREM) sleep, synchronous synaptic activity in the thalamocortical network generates predominantly low-frequency oscillations (< 4 Hz) that are modulated by inhibitory inputs from the thalamic reticular nucleus (TRN). Whether TRN cells integrate sleep-wake signals from subcortical circuits remains unclear. We found that GABA neurons from the lateral hypothalamus (LHGABA) exert a strong inhibitory control over TRN GABA neurons (TRNGABA). We found that optogenetic activation of this circuit recapitulated state-dependent changes of TRN neuron activity in behaving mice and induced rapid arousal during NREM, but not REM, sleep. During deep anesthesia, activation of this circuit induced sustained cortical arousal. In contrast, optogenetic silencing of LHGABA-TRNGABA transmission increased the duration of NREM sleep and amplitude of delta (1-4 Hz) oscillations. Collectively, these results demonstrate that TRN cells integrate subcortical arousal inputs selectively during NREM sleep and may participate in sleep intensity.
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