Abstract

During the transition from neonate to adulthood, brain maturation establishes coherence between behavioral states—wakefulness, non-rapid eye movement, and rapid eye movement sleep. In animal models few studies have characterized and analyzed cerebral rhythms and the sleep–wake cycle in early ages, in relation to adulthood. Since the analysis of sleep in early ages can be used as a predictive model of brain development and the subsequent emergence of neural disturbances in adults, we performed a study on late neonatal mice, an age not previously characterized. We acquired longitudinal 24 h electroencephalogram and electromyogram recordings and performed time and spectral analyses. We compared both age groups and found that late neonates: (i) spent more time in wakefulness and less time in non-rapid eye movement sleep, (ii) showed an increased relative band power in delta, which, however, reduced in theta during each behavioral state, (iii) showed a reduced relative band power in beta during wakefulness and non-rapid eye movement sleep, and (iv) manifested an increased total power over all frequencies. The data presented here might have implications expanding our knowledge of cerebral rhythms in early ages for identification of potential biomarkers in preclinical models of neurodegeneration.

Highlights

  • Sleep is a state of cerebral activity that is regulated by different brain structures, including the hypothalamus, brain stem and basal ganglia

  • In Parkinson’s disease (PD), it is known that neuronal death in the substantia nigra pars compacta (SNpc) is linked to a reduced amount of time spent in rapid eye movement (REM) sleep [6], which is accepted to be a supportive diagnostic criterion, and increased sleep fragmentation has been reported [6,7,8]

  • We confirmed that the percentage of time spent in wakefulness was higher in neonatal than in adult mice, and the opposite occurred in non-rapid eye movement (NREM) sleep (Figure 2A vs. Figure 3A)

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Summary

Introduction

Sleep is a state of cerebral activity that is regulated by different brain structures, including the hypothalamus, brain stem and basal ganglia. Studies in rodents have shown that sleep facilitates neural maturation and prevents apoptosis in developing brains [1,2]. The time spent in REM sleep slowly decreases, while time spent in NREM sleep increases [3,4,5]. In Alzheimer’s disease (AD), the most common cause of dementia in older adults, sleep is highly fragmented, with a circadian disruption leading to daytime hypersomnia and nighttime insomnia. In Parkinson’s disease (PD), it is known that neuronal death in the substantia nigra pars compacta (SNpc) is linked to a reduced amount of time spent in REM sleep [6], which is accepted to be a supportive diagnostic criterion, and increased sleep fragmentation has been reported [6,7,8]

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