Cytokine and microRNA levels during different periods of paradoxical sleep deprivation and sleep recovery in rats

Brianza-Padilla, Malinalli; Sánchez‐Muñoz, Fausto; Vázquez-Palacios, Gonzalo; Huang, Fengyang; Almanza-Perez, Julio César; Bojalil, Rafael; Bonilla-Jaime, Herlinda

doi:10.7717/peerj.5567

Cited by 16 publications

(15 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, another study also comparing the effects of the single and multiple platforms methods, applied during 4 days, on the HPA axis activity of male rats showed that both protocols caused an increased secretion of corticosterone and ACTH, and confirmed that this effect was stronger in the single platform paradigm [138]. The stressful aspect of the multiple platforms apparatus was further highlighted in several other studies showing that 18 h to 21 days of REM-sleep suppression induced an increase in corticosterone and/or ACTH in male rats [139][140][141][142][143][144][145][146][147][148] and mice [149,150]. Other related methods using two small platforms or a 'grid over water' have been shown to also induce an increase in corticosterone in male mice after 2 and 3 days, respectively, [151,152].…”

Section: Do Sleep-deprivation Procedures In Rodentssupporting

confidence: 57%

Sleep deprivation and stress: a reciprocal relationship

2020

View full text Add to dashboard Cite

Sleep is highly conserved across evolution, suggesting vital biological functions that are yet to be fully understood. Animals and humans experiencing partial sleep restriction usually exhibit detrimental physiological responses, while total and prolonged sleep loss could lead to death. The perturbation of sleep homeostasis is usually accompanied by an increase in hypothalamic–pituitary–adrenal (HPA) axis activity, leading to a rise in circulating levels of stress hormones (e.g. cortisol in humans, corticosterone in rodents). Such hormones follow a circadian release pattern under undisturbed conditions and participate in the regulation of sleep. The investigation of the consequences of sleep deprivation, from molecular changes to behavioural alterations, has been used to study the fundamental functions of sleep. However, the reciprocal relationship between sleep and the activity of the HPA axis is problematic when investigating sleep using traditional sleep-deprivation protocols that can induce stress per se . This is especially true in studies using rodents in which sleep deprivation is achieved by exogenous, and potentially stressful, sensory–motor stimulations that can undoubtedly confuse their conclusions. While more research is needed to explore the mechanisms underlying sleep loss and health, avoiding stress as a confounding factor in sleep-deprivation studies is therefore crucial. This review examines the evidence of the intricate links between sleep and stress in the context of experimental sleep deprivation, and proposes a more sophisticated research framework for sleep-deprivation procedures that could benefit from recent progress in biotechnological tools for precise neuromodulation, such as chemogenetics and optogenetics, as well as improved automated real-time sleep-scoring algorithms.

show abstract

Section: Do Sleep-deprivation Procedures In Rodentssupporting

confidence: 57%

Sleep deprivation and stress: a reciprocal relationship

2020

View full text Add to dashboard Cite

show abstract

“…The levels of corticosterone in short-term sleep deprived mice exhibited a mild reduction; these results were consistent with those described in previous studies (Brianza-Padilla et al, 2018). The corticosterone levels of successively sleep-deprived mice has also been reported to increase significantly (Gonzalez-Castañeda et al, 2016; Brianza-Padilla et al, 2018). We also found that the ABR wave I amplitude was temporarily elevated following SD.…”

Section: Discussionsupporting

confidence: 93%

Sleep Deprivation Modifies Noise-Induced Cochlear Injury Related to the Stress Hormone and Autophagy in Female Mice

Dai

Wang

et al. 2019

Front. Neurosci.

View full text Add to dashboard Cite

A lack of sleep is linked with a range of inner ear diseases, including hearing loss and tinnitus. Here, we used a mouse model to investigate the effects of sleep deprivation (SD) on noise vulnerability, and explored the mechanisms that might be involved in vitro, focusing particularly corticosterone levels and autophagic flux in cells. Female BALB/c mice were divided into six groups [control, acoustic trauma (AT)-alone, 1 day (d) SD-alone, 1d SD pre-AT, 5d SD-alone, and 5d SD pre-AT]. Cochlear damage was then assessed by analyzing auditory brainstem response (ABR), and by counting outer hair cells (OHCs) and the synaptic ribbons of inner hair cells (IHCs). In addition, we measured levels of serum corticosterone and autophagy protein expression in the basilar membranes by ELISA kits, and western blotting, respectively. We found that SD-alone temporarily elevated ABR wave I amplitude, but had no permanent effect on hearing level or IHC ribbon numbers. Combined with AT, the number of synaptic ribbons in the 1d SD pre-AT group was significantly higher than that in the AT-alone group, whereas the 5d SD pre-AT group showed more severe synaptopathy, and a greater loss of OHCs after 2 weeks than the other experimental groups exposed to noise. Correspondingly, the levels of corticosterone in the AT-alone group were higher than those of the 1d SD pre-AT group, but lower than those of the 5d SD pre-AT group. The 1d SD pre-AT group showed a marked elevation in the expression of microtubule-associated protein 1 light chain 3B (LC3B), whereas the AT-alone group exhibited only a mild increase. In contrast, the levels of LC3B did not change in the 5d SD pre-AT group. Experiments with HEI-OC-1 cells and cochlear basilar membrane cultures showed that high-concentrations of dexamethasone, and the inhibition of autophagy, aggravated cellular apoptosis induced by oxidative stress. In conclusion, noise-induced synaptopathy and hair cell loss can be mitigated by preceding 1d SD, but will be aggravated by preceding 5d SD. These findings may be attributable to corticosterone levels and the extent of autophagy.

show abstract

“…Many studies in rats support the notion that sleep alterations induce neuroinflammation. Depending on its duration, sleep deprivation can produce multiple physiological effects, including increased plasma corticosterone levels [80][81][82]. This suggests that paradoxical sleep deprivation (PSD) induces a stress response [83] as well as alterations in inflammatory markers, including IL-1β, IL-6, IL-17, and TNF-α [81,84,85], thus contributing to the neuroinflammatory process at the central level [86,87].…”

Section: Animal Studiesmentioning

confidence: 99%

Sleep Disruption Worsens Seizures: Neuroinflammation as a Potential Mechanistic Link

Bonilla-Jaime

Zeleke

Rojas

et al. 2021

IJMS

Self Cite

View full text Add to dashboard Cite

Sleep disturbances, such as insomnia, obstructive sleep apnea, and daytime sleepiness, are common in people diagnosed with epilepsy. These disturbances can be attributed to nocturnal seizures, psychosocial factors, and/or the use of anti-epileptic drugs with sleep-modifying side effects. Epilepsy patients with poor sleep quality have intensified seizure frequency and disease progression compared to their well-rested counterparts. A better understanding of the complex relationship between sleep and epilepsy is needed, since approximately 20% of seizures and more than 90% of sudden unexpected deaths in epilepsy occur during sleep. Emerging studies suggest that neuroinflammation, (e.g., the CNS immune response characterized by the change in expression of inflammatory mediators and glial activation) may be a potential link between sleep deprivation and seizures. Here, we review the mechanisms by which sleep deprivation induces neuroinflammation and propose that neuroinflammation synergizes with seizure activity to worsen neurodegeneration in the epileptic brain. Additionally, we highlight the relevance of sleep interventions, often overlooked by physicians, to manage seizures, prevent epilepsy-related mortality, and improve quality of life.

show abstract

Cytokine and microRNA levels during different periods of paradoxical sleep deprivation and sleep recovery in rats

Cited by 16 publications

References 44 publications

Sleep deprivation and stress: a reciprocal relationship

Sleep deprivation and stress: a reciprocal relationship

Sleep Deprivation Modifies Noise-Induced Cochlear Injury Related to the Stress Hormone and Autophagy in Female Mice

Sleep Disruption Worsens Seizures: Neuroinflammation as a Potential Mechanistic Link

Contact Info

Product

Resources

About