Gerstner Jason R, Flores Carlos C, Lefton Micah, Rogers Brooke, Davis Christopher J
Department of Translational Medicine and Physiology, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA, United States.
Steve Gleason Institute for Neuroscience, Spokane, WA, United States.
Front Syst Neurosci. 2023 Jun 19;17:1212213. doi: 10.3389/fnsys.2023.1212213. eCollection 2023.
Sleep and circadian rhythms are observed broadly throughout animal phyla and influence neural plasticity and cognitive function. However, the few phylogenetically conserved cellular and molecular pathways that are implicated in these processes are largely focused on neuronal cells. Research on these topics has traditionally segregated sleep homeostatic behavior from circadian rest-activity rhythms. Here we posit an alternative perspective, whereby mechanisms underlying the integration of sleep and circadian rhythms that affect behavioral state, plasticity, and cognition reside within glial cells. The brain-type fatty acid binding protein, FABP7, is part of a larger family of lipid chaperone proteins that regulate the subcellular trafficking of fatty acids for a wide range of cellular functions, including gene expression, growth, survival, inflammation, and metabolism. FABP7 is enriched in glial cells of the central nervous system and has been shown to be a clock-controlled gene implicated in sleep/wake regulation and cognitive processing. FABP7 is known to affect gene transcription, cellular outgrowth, and its subcellular localization in the fine perisynaptic astrocytic processes (PAPs) varies based on time-of-day. Future studies determining the effects of FABP7 on behavioral state- and circadian-dependent plasticity and cognitive processes, in addition to functional consequences on cellular and molecular mechanisms related to neural-glial interactions, lipid storage, and blood brain barrier integrity will be important for our knowledge of basic sleep function. Given the comorbidity of sleep disturbance with neurological disorders, these studies will also be important for our understanding of the etiology and pathophysiology of how these diseases affect or are affected by sleep.
睡眠和昼夜节律在整个动物门类中广泛存在,并影响神经可塑性和认知功能。然而,在这些过程中涉及的少数系统发育保守的细胞和分子途径主要集中在神经元细胞上。传统上,关于这些主题的研究将睡眠稳态行为与昼夜休息-活动节律区分开来。在这里,我们提出一种不同的观点,即影响行为状态、可塑性和认知的睡眠与昼夜节律整合的潜在机制存在于神经胶质细胞中。脑型脂肪酸结合蛋白FABP7是脂质伴侣蛋白大家族的一部分,该家族调节脂肪酸的亚细胞运输,以实现广泛的细胞功能,包括基因表达、生长、存活、炎症和代谢。FABP7在中枢神经系统的神经胶质细胞中富集,并已被证明是一个与睡眠/觉醒调节和认知加工有关的生物钟控制基因。已知FABP7会影响基因转录、细胞生长,并且其在精细的突触周围星形胶质细胞突起(PAPs)中的亚细胞定位会随时间变化。未来的研究确定FABP7对行为状态和昼夜节律依赖性可塑性及认知过程的影响,以及对与神经胶质相互作用、脂质储存和血脑屏障完整性相关的细胞和分子机制的功能后果,对于我们了解基本睡眠功能至关重要。鉴于睡眠障碍与神经系统疾病的共病性,这些研究对于我们理解这些疾病如何影响睡眠或受睡眠影响的病因和病理生理学也很重要。