We investigated sleep-wake (S-W) architecture and sleep regulation in the ferret: a phylogenetically primitive mammal increasingly used in neurobiological studies. Twenty-four hour S-W baseline data were collected in eight adult ferrets. Seven ferrets were then sleep deprived for 6h at the beginning of the light period. Like other placental mammals, ferrets exhibited the main vigilance states of wakefulness, rapid-eye-movement (REM) sleep and non-REM (NREM) sleep. Interestingly, the amount of REM sleep in the ferret was considerably higher (24.01+/-1.61% of total recording time) than typically reported in placental mammals. Ferret sleep was homeostatically regulated as sleep deprivation produced a significant increase in NREM EEG delta power during the recovery period. Therefore, ferret sleep in most respects is comparable to sleep in other placental mammals. However, the large amount of REM sleep in this phylogenetically more ancient species suggests that REM sleep may have been present in greater amounts in early stages of mammalian evolution.
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http://dx.doi.org/10.1016/j.bbr.2006.05.001 | DOI Listing |
Entropy (Basel)
January 2025
Departamento de Ingeniería Eléctrica y Computadoras, Instituto de Ciencias e Ingeniería de la Computación, Universidad Nacional del Sur-Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Bahía Blanca 8000, Argentina.
Studying sleep stages is crucial for understanding sleep architecture, which can help identify various health conditions, including insomnia, sleep apnea, and neurodegenerative diseases, allowing for better diagnosis and treatment interventions. In this paper, we explore the effectiveness of generalized weighted permutation entropy (GWPE) in distinguishing between different sleep stages from EEG signals. Using classification algorithms, we evaluate feature sets derived from both standard permutation entropy (PE) and GWPE to determine which set performs better in classifying sleep stages, demonstrating that GWPE significantly enhances sleep stage differentiation, particularly in identifying the transition between N1 and REM sleep.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
National Institute of Biological Sciences, Beijing 102206, China.
Sleep need accumulates during waking and dissipates during sleep to maintain sleep homeostasis (process S). Besides the regulation of daily (baseline) sleep amount, homeostatic sleep regulation commonly refers to the universal phenomenon that sleep deprivation (SD) causes an increase of sleep need, hence, the amount and intensity of subsequent recovery sleep. The central regulators and signaling pathways that govern the baseline and homeostatic sleep regulations in mammals remain unclear.
View Article and Find Full Text PDFSleep Breath
January 2025
Electrical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.
Purpose: The expression of the respiratory events in OSA is influenced by different mechanisms. In particular, REM sleep can highly increase the occurrence of events in a subset of OSA patients, a condition dubbed REM-OSA (often defined as an AHI 2 times higher in REM than NREM sleep). However, a proper characterization of REM-OSA and its pathological sequelae is still inadequate, partly because of limitations in the current definitions.
View Article and Find Full Text PDFRes Sports Med
January 2025
School of Health and Kinesiology, University of Nebraska Omaha, Omaha, USA.
Chronic Ankle Instability (CAI) is a condition characterized by giving-way episodes, instability and recurrent ankle sprains. Poor sleep can increase the risk of musculoskeletal injury and sleep is known to be an important aspect of injury recovery. However, the effect sleep has on those with CAI as well as its risk for recurrent episodes of giving-way remains unclear.
View Article and Find Full Text PDFAnn Clin Transl Neurol
January 2025
Section of Pediatric Neurology and Developmental Neuroscience, Department of Pediatrics, Baylor College of Medicine, Houston, Texas, 77030, USA.
Objective: Rett syndrome (RTT) and MECP2 duplication syndrome (MDS) result from under- and overexpression of MECP2, respectively. Preclinical studies using genetic-based treatment showed robust phenotype recovery for both MDS and RTT. However, there is a risk of converting MDS to RTT, or vice versa, if accurate MeCP2 levels are not achieved.
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