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A role for orexin in central vestibular motor control.食欲素在中枢前庭运动控制中的作用。
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2
Respiratory regulation in narcolepsy.发作性睡病的呼吸调节。
Sleep Breath. 2012 Mar;16(1):241-5. doi: 10.1007/s11325-011-0489-x. Epub 2011 Feb 12.
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Orexin/hypocretin plays a role in the response to physiological disequilibrium.食欲素/下丘脑分泌素在对生理失衡的反应中起作用。
Sleep Med Rev. 2011 Jun;15(3):197-207. doi: 10.1016/j.smrv.2010.12.003. Epub 2011 Jan 26.
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Effect of orexin-A on post-ischemic glucose intolerance and neuronal damage.orexin-A 对缺血后葡萄糖不耐受和神经元损伤的影响。
J Pharmacol Sci. 2011;115(2):155-63. doi: 10.1254/jphs.10264fp. Epub 2011 Jan 18.
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Orexins/hypocretins increase the promoter activity of selective steroidogenic enzymes.食欲肽/下丘脑分泌素增加选择性甾体生成酶的启动子活性。
Peptides. 2011 Apr;32(4):839-43. doi: 10.1016/j.peptides.2011.01.004. Epub 2011 Jan 20.
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Neuroprotective effect of orexin-A is mediated by an increase of hypoxia-inducible factor-1 activity in rat.神经肽 orexin-A 通过增加低氧诱导因子-1 活性发挥神经保护作用。
Anesthesiology. 2011 Feb;114(2):340-54. doi: 10.1097/ALN.0b013e318206ff6f.
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Direct and indirect control of orexin/hypocretin neurons by glycine receptors.甘氨酸受体对食欲素/下丘脑分泌素神经元的直接和间接控制。
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8
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Orexin/hypocretin modulates response of ventral tegmental dopamine neurons to prefrontal activation: diurnal influences.食欲素/下丘脑分泌素调节腹侧被盖区多巴胺神经元对前额叶激活的反应:昼夜节律的影响。
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Sleeping through the night: the consolidation of self-regulated sleep across the first year of life.整夜睡眠:生命第一年自我调节睡眠的巩固。
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脑脊液中下丘脑泌素-1(食欲素-A)的水平在人类婴儿期早期达到峰值。

CSF levels of hypocretin-1 (orexin-A) peak during early infancy in humans.

机构信息

Neuropediatric Unit, Shaare Zedek Medical Center, Hebrew University, Jerusalem, Israel.

出版信息

Sleep. 2012 Feb 1;35(2):187-91. doi: 10.5665/sleep.1618.

DOI:10.5665/sleep.1618
PMID:22294808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3250357/
Abstract

STUDY OBJECTIVES

Hypocretin (orexin) is a unique neuropeptide involved in the consolidation of wakefulness and sleep. Although hypocretin-1 levels in the cerebrospinal fluid (CSF) are stable after infancy, how levels change in preterm and term human infants is unknown.

DESIGN, PATIENTS, AND SETTING: Hypocretin-1 levels were measured in CSF samples, obtained from 284 preterm (25-37 gestational weeks) and full-term infants in the first 4 months of life and 35 older children (ages 0.5-13 years), in a tertiary hospital.

MEASUREMENTS AND RESULTS

Detailed clinical and laboratory data were collected for each of the 319 participants. Based on that data, 108 neurologically intact children were selected (95 infants [43 preterm and 52 term] and 13 older children). CSF hypocretin-1 was measured by direct radioimmunoassay. Hypocretin-1 levels at the first weeks of the 3rd embryonic trimester (gestational age [GA] 28-34 weeks) were 314 ± 65 pg/mL (n = 17). The levels linearly increased during the third trimester and early infancy (r = 0.6), peaking in infants of 2-4 months ages (476 ± 72 pg/mL; n = 16) and decreasing thereafter; hypocretin levels in 2- to 4-month-old infants were significantly higher than those in children 0.5-13 years old (353 ± 78 pg/mL, n = 13; P = 0.0001).

CONCLUSIONS

The present findings indicate that in human infants, CSF hypocretin-1 increases during the third embryonic trimester and is highest at 4 months of life. Thereafter, and consistent with previously published results, hypocretin levels are lower and stable until the geriatric age. This pattern may reflect the role of hypocretin in the dramatic process of sleep and wakefulness consolidation that occurs during early infancy.

摘要

研究目的

食欲肽(orexin)是一种参与觉醒和睡眠巩固的独特神经肽。尽管脑脊液(CSF)中的食欲肽-1 水平在婴儿期后保持稳定,但早产儿和足月儿人类婴儿的水平如何变化尚不清楚。

设计、患者和环境:在一家三级医院,测量了 284 名早产儿(25-37 孕周)和足月儿婴儿在生命的前 4 个月以及 35 名年龄较大的儿童(0.5-13 岁)的 CSF 样本中的食欲肽-1 水平。

测量和结果

为 319 名参与者中的每一位都收集了详细的临床和实验室数据。基于这些数据,选择了 108 名神经完整的儿童(95 名婴儿[43 名早产儿和 52 名足月儿]和 13 名年龄较大的儿童)。通过直接放射免疫测定法测量 CSF 食欲肽-1。第 3 个胚胎期(孕龄 [GA] 28-34 周)的前几周的食欲肽-1 水平为 314 ± 65 pg/mL(n = 17)。水平在第三个三个月和婴儿早期呈线性增加(r = 0.6),在 2-4 个月龄的婴儿中达到峰值(476 ± 72 pg/mL;n = 16),此后下降;2-4 个月龄婴儿的食欲肽水平明显高于 0.5-13 岁儿童(353 ± 78 pg/mL,n = 13;P = 0.0001)。

结论

本研究结果表明,在人类婴儿中,CSF 食欲肽-1 在第三个胚胎期增加,在 4 个月龄时达到最高。此后,与先前发表的结果一致,食欲肽水平较低且稳定,直到老年。这种模式可能反映了食欲肽在婴儿早期睡眠和觉醒巩固的剧烈过程中的作用。