Variabilidade individual da sonolência de camundongos submetidos à privação de sono aguda e crônica

• Ano de defesa: 2019
• Autor(a) principal: Fernandes, Guilherme Luiz [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Sleep homeostasis; Sleepiness; Sleep deprivation; Homeostase do sono; Sonolência; Privação de sono
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=8295189; https://repositorio.unifesp.br/handle/11600/58746

Introduction: Homeostatic sleep regulation has molecular markers, such as the adenosine-5’-triphosphate P2X7 and glutamate AMPAR receptors, or behavioral, such as sleep need, shown by sleepiness. However, there is a lack of evidence linking sleep need with the molecular mechanisms of homeostasis, which could be tested by acute and chronic sleep deprivation. Objectives: To investigate the development and related factors of sleepiness in sleep deprived mice. Methods: C57BL/6J mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 h after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results: Using the average group sleep attempts, it was possible to differentiate between sleepy (mean> group average) and resistant to sleepiness animals (mean < group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12h of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation could be attributed to extended wakefulness. 6 h of acute sleep deprivation lowered plasmatic corticosterone. Conclusions: Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant.