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首页> 外文期刊>Brain, Behavior, and Immunity >Differential activation of immune factors in neurons and glia contribute to individual differences in resilience/vulnerability to sleep disruption
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Differential activation of immune factors in neurons and glia contribute to individual differences in resilience/vulnerability to sleep disruption

机译:神经元和神经胶质细胞中免疫因子的差异激活导致个体抵抗力/睡眠障碍脆弱性的差异

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摘要

Individuals frequently find themselves confronted with a variety of challenges that threaten their wellbeing. While some individuals face these challenges efficiently and thrive (resilient) others are unable to cope and may suffer persistent consequences (vulnerable). Resilience/vulnerability to sleep disruption may contribute to the vulnerability of individuals exposed to challenging conditions. With that in mind we exploited individual differences in a fly's ability to form short-term memory (STM) following 3 different types of sleep disruption to identify the underlying genes. Our analysis showed that in each category of flies examined, there are individuals that form STM in the face of sleep loss (resilient) while other individuals show dramatic declines in cognitive behavior (vulnerable). Molecular genetic studies revealed that Antimicrobial Peptides, factors important for innate immunity, were candidates for conferring resilience/vulnerability to sleep deprivation. Specifically, Metchnikowin (Mtk), drosocin (dro) and Attacin (Att) transcript levels seemed to be differentially increased by sleep deprivation in glia (Mtk), neurons (dro) or primarily in the head fat body (Aft). Follow-up genetic studies confirmed that expressing Mtk in glia but not neurons, and expressing dro in neurons but not glia, disrupted memory while modulating sleep in opposite directions. These data indicate that various factors within glia or neurons can contribute to individual differences in resilience/vulnerability to sleep deprivation. (C) 2014 Elsevier Inc. All rights reserved.
机译:个人经常发现自己面临着各种威胁其健康的挑战。尽管有些人有效地应对这些挑战并蓬勃发展(弹性),但另一些人却无法应对,并可能遭受持续的后果(脆弱)。抵抗睡眠的弹性/脆弱性可能会导致面临挑战的个人易受伤害。考虑到这一点,我们利用苍蝇在3种不同类型的睡眠中断后形成短期记忆(STM)的能力上的个体差异来识别潜在的基因。我们的分析表明,在所检查的每类苍蝇中,都有面对睡眠不足(有弹性)而形成STM的个体,而其他个体则表现出认知行为的急剧下降(易受伤害)。分子遗传学研究表明,抗菌肽是先天免疫的重要因素,是赋予睡眠剥夺弹性/脆弱性的候选药物。具体而言,胶质瘤(Mtk),神经元(dro)或主要在头脂肪体(Aft)中的睡眠剥夺似乎使Metchnikowin(Mtk),drosocin(dro)和Attacin(Att)转录水平有所不同。后续的遗传研究证实,在神经胶质而不是神经元中表达Mtk,在神经元而不是神经胶质中表达dro,在调节睡眠的相反方向时会破坏记忆。这些数据表明,神经胶质细胞或神经元内的各种因素可导致睡眠剥夺的弹性/脆弱性方面的个体差异。 (C)2014 Elsevier Inc.保留所有权利。

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