Abstract:Behavioral states alternate between wakefulness (wk), rapid eye movement (rem) and non-rem (nrem) sleep at time scale of hours i.e., light and dark cycle rhythms and from several tens of minutes to seconds (i.e., brief awakenings during sleep). Using statistical analysis of bout duration, Markov chains of sleep-wk dynamics and quantitative EEG analysis, we evaluated the influence of light/dark (ld) changes on brain function along the sleep-wk cycle. Bout duration (bd) histograms and Kaplan-Meier (km) survival … Show more
“…Figure 5B depicts the probability of transitioning between/within states of wakefulness, NREM sleep and REM sleep. Consistent with a previous study (Perez-Atencio et al, 2018), the probability of remaining in one state was much higher injection. Figure 5D shows that the activation of glutamatergic neurons of the medial-lateral preoptic region significantly altered the probability distribution of bout duration by increasing the number of short bouts and decreasing the number of long bouts during both NREM sleep (p < 0.0001) and wakefulness (p < 0.0001).…”
Section: Activation Of Medial-lateral Preoptic Glutamatergic Neurons supporting
Glutamatergic neurons in the preoptic hypothalamus promote wakefulness, destabilize NREM sleep, suppress REM sleep, and regulate cortical dynamics Abbreviated tittle: Wake and EEG control by preoptic Vglut2+ neurons
“…Figure 5B depicts the probability of transitioning between/within states of wakefulness, NREM sleep and REM sleep. Consistent with a previous study (Perez-Atencio et al, 2018), the probability of remaining in one state was much higher injection. Figure 5D shows that the activation of glutamatergic neurons of the medial-lateral preoptic region significantly altered the probability distribution of bout duration by increasing the number of short bouts and decreasing the number of long bouts during both NREM sleep (p < 0.0001) and wakefulness (p < 0.0001).…”
Section: Activation Of Medial-lateral Preoptic Glutamatergic Neurons supporting
Glutamatergic neurons in the preoptic hypothalamus promote wakefulness, destabilize NREM sleep, suppress REM sleep, and regulate cortical dynamics Abbreviated tittle: Wake and EEG control by preoptic Vglut2+ neurons
“…Figure 7A depicts the probability of transitioning between/within states of wakefulness, NREM sleep and REM sleep. Consistent with a previous study (Perez-Atencio et al, 2018), the probability of remaining in one state was much higher than the probability of transitioning into a Second, to evaluate the stability of sleep-wake states in each 1-hour block, we calculated a fragmentation index (FI); FI = 1 indicates that the state is maximally unstable and fragmented. Because of the scarcity of REM sleep after CNO administration, we only performed this analysis for wakefulness and NREM sleep states.…”
Section: Activation Of Medial-lateral Preoptic Glutamatergic Neurons mentioning
Clinical and experimental data from the last nine decades indicate that the preoptic area of the hypothalamus is a critical node in a brain network that controls sleep onset and homeostasis. By contrast, we recently reported that a group of glutamatergic neurons in the lateral and medial preoptic area increases wakefulness, challenging the long-standing notion in sleep neurobiology that the preoptic area is exclusively somnogenic. However, the precise role of these subcortical neurons in the control of behavioral state transitions and cortical dynamics remains unknown. Therefore, in this study we used conditional expression of excitatory hM3Dq receptors in these preoptic glutamatergic (Vglut2+) neurons and show that their activation initiates wakefulness, decreases non-rapid eye movement (NREM) sleep, and causes a persistent suppression of rapid eye movement (REM) sleep. Activation of preoptic glutamatergic neurons also causes a high degree of NREM sleep fragmentation, promotes state instability with frequent arousals from sleep, and shifts cortical dynamics (including oscillations, connectivity, and complexity) to a more wake-like state. We conclude that a subset of preoptic glutamatergic neurons may initiate (but not maintain) arousals from sleep, and their inactivation may be required for NREM stability and REM sleep generation. Further, these data provide novel empirical evidence supporting the conclusion that the preoptic area causally contributes to the regulation of both sleep and wakefulness.
“…In humans, sleep is regulated both by the intensity of the drive to fall asleep (higher in narcolepsy, lower in insomnia) and the tendency to wake up (higher in insomnia, lower in hypersomnolence and depression) (Barateau et al 2017; Kales and Kales 1974). To capture these drives, conditional probability models using neuronal firing or EEG data have been used to model the structure of healthy and disordered sleep in mammals (Bianchi et al 2012; Perez-Atencio et al 2018; Stephenson et al 2016; Yang and Hursch 1973), but this approach had not yet been applied to sleep in Drosophila .…”
Acknowledgements
25We would like to thank Dr. Jané Kondev and the students in the Brandeis Quantitative
26Biology Research Community (QBReC) who assisted in collecting preliminary data.
28
Grants
30This work was funded by R01 MH067284 (to LCG) and F32 NS098624 (to TDW).
32. CC-BY-NC-ND 4.0 International license It is made available under a (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The copyright holder for this preprint . http://dx.doi.org/10.1101/263301 doi: bioRxiv preprint first posted online Feb. 12, 2018;
2
ABSTRACT
33In humans and flies, sleep is a highly organized behavior, occurring in discrete bouts 34 that are consolidated at night but have a more fragmented structure during the day.
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