Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle
Sleep is a fundamental homeostatic process within the animal kingdom. Although various brain areas and cell types are involved in the regulation of the sleep–wake cycle, it is still unclear how different pathways between neural populations contribute to its regulation. Here we address this issue by...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2019-12-01
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Series: | Frontiers in Neuroscience |
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Online Access: | https://www.frontiersin.org/article/10.3389/fnins.2019.01380/full |
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author | Charlotte Héricé Shuzo Sakata |
author_facet | Charlotte Héricé Shuzo Sakata |
author_sort | Charlotte Héricé |
collection | DOAJ |
description | Sleep is a fundamental homeostatic process within the animal kingdom. Although various brain areas and cell types are involved in the regulation of the sleep–wake cycle, it is still unclear how different pathways between neural populations contribute to its regulation. Here we address this issue by investigating the behavior of a simplified network model upon synaptic weight manipulations. Our model consists of three neural populations connected by excitatory and inhibitory synapses. Activity in each population is described by a firing-rate model, which determines the state of the network. Namely wakefulness, rapid eye movement (REM) sleep or non-REM (NREM) sleep. By systematically manipulating the synaptic weight of every pathway, we show that even this simplified model exhibits non-trivial behaviors: for example, the wake-promoting population contributes not just to the induction and maintenance of wakefulness, but also to sleep induction. Although a recurrent excitatory connection of the REM-promoting population is essential for REM sleep genesis, this recurrent connection does not necessarily contribute to the maintenance of REM sleep. The duration of NREM sleep can be shortened or extended by changes in the synaptic strength of the pathways from the NREM-promoting population. In some cases, there is an optimal range of synaptic strengths that affect a particular state, implying that the amount of manipulations, not just direction (i.e., activation or inactivation), needs to be taken into account. These results demonstrate pathway-dependent regulation of sleep dynamics and highlight the importance of systems-level quantitative approaches for sleep–wake regulatory circuits. |
first_indexed | 2024-12-11T11:11:41Z |
format | Article |
id | doaj.art-9a266642cc72409e9e7b3fae6b7e6937 |
institution | Directory Open Access Journal |
issn | 1662-453X |
language | English |
last_indexed | 2024-12-11T11:11:41Z |
publishDate | 2019-12-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Neuroscience |
spelling | doaj.art-9a266642cc72409e9e7b3fae6b7e69372022-12-22T01:09:30ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2019-12-011310.3389/fnins.2019.01380497195Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake CycleCharlotte HéricéShuzo SakataSleep is a fundamental homeostatic process within the animal kingdom. Although various brain areas and cell types are involved in the regulation of the sleep–wake cycle, it is still unclear how different pathways between neural populations contribute to its regulation. Here we address this issue by investigating the behavior of a simplified network model upon synaptic weight manipulations. Our model consists of three neural populations connected by excitatory and inhibitory synapses. Activity in each population is described by a firing-rate model, which determines the state of the network. Namely wakefulness, rapid eye movement (REM) sleep or non-REM (NREM) sleep. By systematically manipulating the synaptic weight of every pathway, we show that even this simplified model exhibits non-trivial behaviors: for example, the wake-promoting population contributes not just to the induction and maintenance of wakefulness, but also to sleep induction. Although a recurrent excitatory connection of the REM-promoting population is essential for REM sleep genesis, this recurrent connection does not necessarily contribute to the maintenance of REM sleep. The duration of NREM sleep can be shortened or extended by changes in the synaptic strength of the pathways from the NREM-promoting population. In some cases, there is an optimal range of synaptic strengths that affect a particular state, implying that the amount of manipulations, not just direction (i.e., activation or inactivation), needs to be taken into account. These results demonstrate pathway-dependent regulation of sleep dynamics and highlight the importance of systems-level quantitative approaches for sleep–wake regulatory circuits.https://www.frontiersin.org/article/10.3389/fnins.2019.01380/fullsleep regulatory circuitscomputational modelbrain statesleep/wake cyclePython programing language |
spellingShingle | Charlotte Héricé Shuzo Sakata Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle Frontiers in Neuroscience sleep regulatory circuits computational model brain state sleep/wake cycle Python programing language |
title | Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle |
title_full | Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle |
title_fullStr | Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle |
title_full_unstemmed | Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle |
title_short | Pathway-Dependent Regulation of Sleep Dynamics in a Network Model of the Sleep–Wake Cycle |
title_sort | pathway dependent regulation of sleep dynamics in a network model of the sleep wake cycle |
topic | sleep regulatory circuits computational model brain state sleep/wake cycle Python programing language |
url | https://www.frontiersin.org/article/10.3389/fnins.2019.01380/full |
work_keys_str_mv | AT charlotteherice pathwaydependentregulationofsleepdynamicsinanetworkmodelofthesleepwakecycle AT shuzosakata pathwaydependentregulationofsleepdynamicsinanetworkmodelofthesleepwakecycle |