Topchiy Irina, Amodeo Dionisio A, Ragozzino Michael E, Waxman Jonathan, Radulovacki Miodrag, Carley David W
Center for Narcolepsy, Sleep and Health Research, University of Illinois at Chicago, Chicago, IL ; Department of Biobehavioral and Health Sciences, University of Illinois at Chicago, Chicago, IL.
Department of Psychology, University of Illinois at Chicago, Chicago, IL.
Sleep. 2014 Nov 1;37(11):1851-61. doi: 10.5665/sleep.4184.
To determine whether learning deficits occur during acute exacerbation of spontaneous sleep related breathing disorder (SRBD) in rats with high (Brown Norway; BN) and low (Zucker Lean; ZL) apnea propensity.
Spatial acquisition (3 days) and reversal learning (3 days) in the Morris water maze (MWM) with polysomnography (12:00-08:00): (1) with acute SRBD exacerbation (by 20-h hyperoxia immediately preceding reversal learning) or (2) without SRBD exacerbation (room air throughout).
Randomized, placebo-controlled, repeated-measures design.
14 BN rats; 16 ZL rats.
20-h hyperoxia.
Apneas were detected as cessation of respiration ≥ 2 sec. Swim latency in MWM, apnea indices (AI; apneas/hour of sleep) and percentages of recording time for nonrapid eye movement (NREM), rapid eye movement (REM), and total sleep were assessed. Baseline AI in BN rats was more than double that of ZL rats (22.46 ± 2.27 versus 10.7 ± 0.9, P = 0.005). Hyperoxia increased AI in both BN (34.3 ± 7.4 versus 22.46 ± 2.27) and ZL rats (15.4 ± 2.7 versus 10.7 ± 0.9) without changes in sleep stage percentages. Control (room air) BN and ZL rats exhibited equivalent acquisition and reversal learning. Acute exacerbation of AI by hyperoxia produced a reversal learning performance deficit in BN but not ZL rats. In addition, the percentage of REM sleep and REM apnea index in BN rats during hyperoxia negatively correlated with reversal learning performance.
Acute exacerbation of sleep related breathing disorder by hyperoxia impairs reversal learning in a rat strain with high apnea propensity, but not a strain with a low apnea propensity. This suggests a non-linear threshold effect may contribute to the relationships between sleep apnea and cognitive dysfunctions, but strain-specific differences also may be important.
确定在自发性睡眠相关呼吸障碍(SRBD)急性加重期间,高呼吸暂停倾向(布朗挪威大鼠;BN)和低呼吸暂停倾向( Zucker 瘦型大鼠;ZL)的大鼠是否会出现学习缺陷。
在莫里斯水迷宫(MWM)中进行空间学习(3天)和逆向学习(3天),同时进行多导睡眠图监测(12:00 - 08:00):(1)伴有SRBD急性加重(在逆向学习前立即进行20小时高氧处理)或(2)无SRBD加重(全程置于室内空气中)。
随机、安慰剂对照、重复测量设计。
14只BN大鼠;16只ZL大鼠。
20小时高氧处理。
呼吸暂停定义为呼吸停止≥2秒。评估在MWM中的游泳潜伏期、呼吸暂停指数(AI;每小时睡眠时间中的呼吸暂停次数)以及非快速眼动(NREM)、快速眼动(REM)和总睡眠时间的记录时间百分比。BN大鼠的基线AI是ZL大鼠的两倍多(22.46±2.27对10.7±0.9,P = 0.005)。高氧处理使BN大鼠(34.3±7.4对22.46±2.27)和ZL大鼠(15.4±2.7对10.7±0.9)的AI均增加,而睡眠阶段百分比无变化。对照(室内空气)组的BN和ZL大鼠表现出相当的学习和逆向学习能力。高氧导致的AI急性加重使BN大鼠出现逆向学习性能缺陷,但ZL大鼠未出现。此外,高氧处理期间BN大鼠的REM睡眠百分比和REM呼吸暂停指数与逆向学习性能呈负相关。
高氧导致的睡眠相关呼吸障碍急性加重会损害高呼吸暂停倾向大鼠品系的逆向学习能力,但不会损害低呼吸暂停倾向大鼠品系的逆向学习能力。这表明非线性阈值效应可能在睡眠呼吸暂停与认知功能障碍的关系中起作用,但品系特异性差异也可能很重要。