Abstract
Recent studies have identified the Drosophila brain circuits involved in the sleep/wake switch and have pointed to the modulation of neuronal excitability as one of the underlying mechanisms triggering sleep need. In this study we aimed to explore the link between the homeostatic regulation of neuronal excitability and sleep behavior in the circadian circuit. For this purpose, we selected Pumilio (Pum), whose main function is to repress protein translation and has been linked to modulation of neuronal excitability during chronic patterns of altered neuronal activity. Here we explore the effects of Pum on sleep homeostasis in Drosophila melanogaster, which shares most of the major features of mammalian sleep homeostasis. Our evidence indicates that Pum is necessary for sleep rebound and that its effect is more pronounced during chronic sleep deprivation (84 h) than acute deprivation (12 h). Knockdown of pum, results in a reduction of sleep rebound during acute sleep deprivation and the complete abolishment of sleep rebound during chronic sleep deprivation. Based on these findings, we propose that Pum is a critical regulator of sleep homeostasis through neural adaptations triggered during sleep deprivation.
Highlights
IntroductionEven by our own experience, that the urge to sleep increases as a function of time awake
It is well established, even by our own experience, that the urge to sleep increases as a function of time awake
In this study we decided to explore the role of pum in the regulation of sleep homeostasis induced by chronic sleep deprivation as well as acute sleep deprivation (SD)
Summary
Even by our own experience, that the urge to sleep increases as a function of time awake This urge, or sleep drive, triggers a prolonged compensatory sleep after the organism is sleep deprived (Daan et al, 1984; Allada, et al, 2017). This compensatory sleep, which is called sleep rebound, is a key indicator of the homeostatic regulation of sleep (Vyazovskiy, et al, 2009). To achieve that level of understanding, we need to study the link between molecular markers, sleep brain circuits and homeostatic sleep behavior
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