College of Veterinary Medicine and BK21 FOUR Program, Chonnam National University, 61186 Gwangju, Republic of Korea.
Department of Nephrology, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Integr Neurosci. 2024 Aug 13;23(8):144. doi: 10.31083/j.jin2308144.
Sleep disorders are prevalent neurological conditions linked to neurocognitive impairments. Understanding the neuroplasticity changes in the hippocampus, which plays a central role in regulating neurocognitive function, is crucial in the context of sleep disorders. However, research on neurodegenerative disorders and the influence of sleep disorders on hippocampal neuroplasticity remains largely unclear. Therefore, this review aims to highlight the latest advancements regarding hippocampal neuroplasticity and functional changes during sleep disorders, drawing insights from clinical and preclinical research involving sleep-deprived animal models. These articles were gathered through comprehensive literature searches across databases, including Google Scholar, PubMed, Web of Science, and Scopus. Maternal sleep deprivation has been observed to cause neurocognitive impairment in offspring, along with changes in protein expression levels associated with neuroplasticity. Similarly, sleep deprivation in adult mice has been shown to affect several cognitive functions and fear extinction without influencing the acquisition of fear conditioning. While mechanistic research on neurocognitive dysfunction induced by maternal and adult sleep deprivation is limited, it suggests the involvement of several signaling pathways, including neurotrophic factors, synaptic proteins, and inflammatory molecules, which are triggered by sleep deprivation. Further studies are needed to clarify the mechanistic pathways underlying hippocampal dysfunction and synaptic alterations associated with sleep disturbances.
睡眠障碍是常见的神经紊乱疾病,与神经认知障碍有关。了解在调节神经认知功能方面起核心作用的海马体的神经可塑性变化,对于睡眠障碍至关重要。然而,关于神经退行性疾病的研究以及睡眠障碍对海马体神经可塑性的影响在很大程度上仍不清楚。因此,本综述旨在强调睡眠障碍期间海马体神经可塑性和功能变化的最新进展,从涉及睡眠剥夺动物模型的临床和临床前研究中汲取见解。这些文章是通过在包括 Google Scholar、PubMed、Web of Science 和 Scopus 在内的数据库中进行全面文献搜索收集的。已经观察到母体睡眠剥夺会导致后代的神经认知障碍,以及与神经可塑性相关的蛋白质表达水平的变化。同样,在成年小鼠中进行的睡眠剥夺已被证明会影响几种认知功能和恐惧消退,而不会影响恐惧条件反射的获得。虽然关于母体和成年睡眠剥夺引起的神经认知功能障碍的机制研究有限,但它表明涉及几种信号通路,包括神经营养因子、突触蛋白和炎症分子,这些通路是由睡眠剥夺引发的。需要进一步的研究来阐明与睡眠障碍相关的海马体功能障碍和突触改变的机制途径。