Navegando por Palavras-chave "Sleep homeostasis"
- ItemSomente MetadadadosChronic stress during paradoxical sleep deprivation increases paradoxical sleep rebound: Association with prolactin plasma levels and brain serotonin content(Elsevier B.V., 2008-10-01) Machado, Ricardo Borges [UNIFESP]; Tufik, Sergio [UNIFESP]; Suchecki, Deborah [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Previous studies suggest that stress associated to steep deprivation methods can affect the expression of steep rebound. in order to examine this association and possible mechanisms, rats were exposed to footshock stress during or immediately after a 96-h period of paradoxical steep deprivation (PSD) and their steep and heart rate were recorded. Control rats (maintained in individual home cages) and paradoxical steep-deprived (PS-deprived) rats were distributed in three conditions (1) no footshock - NF; (2) single footshock - SFS: one single footshock session at the end of the PSD period (6-8 shocks per minute; 100 ms; 2 mA; for 40 min); and (3) multiple footshock - MFS: footshock sessions with the same characteristics as described above, twice a day throughout PSD (at 7:00 h and 19:00 h) and one extra session before the recovery period. After PSD, animals were allowed to sleep freely for 72 h. Additional groups were sacrificed at the end of the steep deprivation period for blood sampling (ACTH, corticosterone, protactin and catecholamine levels) and brain harvesting (monoamines and metabolites). Neither SFS nor MFS produced significant alterations in the steep patterns of control rats. All PS-deprived groups exhibited increased heart rate which could be explained by increased dopaminergic activity in the medulla. As expected, PS deprivation induced rebound of paradoxical steep in the first day of recovery; however, PSD + MFS group showed the highest rebound (327.3% above the baseline). This group also showed intermediate Levels of corticosterone and the highest levels of protactin, which were positively correlated with the Length of PS episodes. Moreover, paradoxical steep deprivation resulted in elevation of the serotonergic turnover in the hypothalamus, which partly explained the hormonal results, and in the hippocampus, which appears to be related to adaptive responses to stress. the data are discussed in the realm of a prospective importance of paradoxical steep for processing of traumatic events. (C) 2008 Elsevier B.V. ALL rights reserved.
- ItemAcesso aberto (Open Access)Variabilidade individual da sonolência de camundongos submetidos à privação de sono aguda e crônica(Universidade Federal de São Paulo (UNIFESP), 2019-11-28) Fernandes, Guilherme Luiz [UNIFESP]; Andersen, Monica Levy [UNIFESP]; http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4794093P4; http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4639440Z0; Universidade Federal de São Paulo (UNIFESP)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.