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Recent studies have identified the 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 , 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 , 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.

Recent research has added a wealth of knowledge towards our understanding of the molecular and cellular mechanisms regulating sleep. However, the mechanisms responsible for compensatory sleep —specifically those elicited in response to long-term (chronic) sleep deprivation— remain largely unexplored. In this study, we show for the first time that the translational repressor Pumilio is an important regulator of the compensatory sleep homeostasis. Moreover, this is the first study in Drosophila exploring the compensatory mechanisms of chronic sleep deprivation, as opposed to acute deprivation. We demonstrate that the response elicited by acute and chronic sleep deprivation are indeed different—both behaviorally and molecularly. In addition, we demonstrate that Pumilio also regulates the homeostatic response to temperature increase during sleep. Furthermore, we provide evidence supporting the notion that translational regulation, effected through the target of Rapamycin (TOR) pathway, also play a relevant role in compensatory sleep regulation. Given the high prevalence of chronic sleep deprivation in our society, its wide range of negative consequences, and the evolutionary conservation of Pumilio, we believe that our findings are quite important and of great interest to the scientific community.

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 the neuronal homeostasis protein 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 hours) than acute deprivation (12 hours). 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. These behavioral changes were associated with accompanying changes in the expression of genes involved in the regulation of neuronal excitability. Interestingly, pum knockdown also increased baseline daytime sleep, suggesting that Pum differentially regulates rebound and normal sleep. Based on these findings, we propose that Pum is a critical regulator of sleep homeostasis through neural adaptations triggered during sleep deprivation and induces rebound sleep by altering neuronal excitability.

El alumnado de los conservatorios se enfrenta con relativa frecuencia a problemas tales como el miedo escénico, la ansiedad, la desmotivación o bloqueos en el proceso creativo, que pueden frenar su desarrollo musical y poner en riesgo su salud. La Musicoterapia puede ser una herramienta clave para prevenir y mitigar estos factores, en aras del bienestar de los estudiantes.  Diseñamos un programa de musicoterapia de improvisación en el que participaron nueve estudiantes en los últimos cursos de las Enseñanzas Profesionales de Música, asistiendo a un total de diez sesiones de hora y media de duración. Analizamos las percepciones de los participantes sobre el proceso mediante la realización de entrevistas individuales y la distribución de cuestionarios anónimos. Los resultados revelaron un muy alto nivel de satisfacción de los discentes, quienes destacaron cómo el proceso terapéutico favoreció especialmente la socialización en el grupo, el disfrute a través de la música, el autoconocimiento y la capacidad de escucha.   

El alumnado de los conservatorios se enfrenta con relativa frecuencia a problemas tales como el miedo escénico, la ansiedad, la desmotivación o bloqueos en el proceso creativo, que pueden frenar su desarrollo musical y poner en riesgo su salud. La Musicoterapia puede ser una herramienta clave para prevenir y mitigar estos factores, en aras del bienestar de los estudiantes.