人参皂甙对大鼠自发睡眠结构的影响机制

 摘要：目的 研究人参皂甙（GS）调节自然睡眠的作用机制。方法 雄性SD大鼠随机分为对照、GS低(10 mg/kg)和高（100 mg/kg）剂量组。在大鼠体内植入无线发射器,术后按10和100mg/ kg GS或蒸馏水每日1次给大鼠灌胃,共6天。第1（急性）和6天（慢性）给药后,开始记录自由活动大鼠脑电活动12 h。在并列进行的另一个实验中,于大鼠给药第1和6天用乙醚麻醉后断头处死,取下丘脑组织检测GABAAergic系统蛋白表达情况。结果 GS 灌胃第1天,低剂量GS略微（P?>0.05）而高剂量显著增加非快动眼睡眠（NREM）和总睡眠而减少觉醒时间（P? <0.05）; 与对照组相比,GS低和高剂量均未改变大鼠下丘脑GAD蛋白表达（P? >0.05）,但都增强了GABAA受体α、?亚型而没有影响?亚型表达（P? <0.05）。连续灌胃第6天,低、高剂量GS均显著增加NREM和总睡眠,减少觉醒（P? <0.05）;同时低剂量GS略微上调低剂量GS略微（P?>0.05）而高剂量GS显著增强大鼠下丘脑GAD蛋白表达水平（P? <0.05）,但低、高剂量GS均未能影响GABAA受体表达（P? >0.05）。结论 GS能时间和剂量依赖性地调节大鼠的自然睡眠结构,其急性作用可能与下丘脑增加的GABAA受体α、?亚型蛋白表达有关,而慢性作用可能涉及经由上调GAD表达水平增加GABA产量。     

可卡因戒断对大鼠睡眠结构和脑电功率谱的影响

目的: 探索可卡因戒断对睡眠觉醒活动的影响。方法: 大鼠体内植入无线发射器,用药前、停药第1 d(急性)、8 d(亚急性)、14 d(亚慢性)记录自由活动大鼠脑电波24 h。结果: 停药第1 d睡眠觉醒周期上升(P<0.05)。停药第8 d夜晚和白天,非快动眼睡眠(NREM)增加(P<0.05),快动眼睡眠(REM)下降(P<0.01);停药第14 d,NREM睡眠夜晚显著增加(P<0.01)而白天仅略加强,白天和夜间REM睡眠均明显下降(P<0.01)。停药期间白天和夜间总睡眠无明显变化。整个实验期间,NREM、REM睡眠和觉醒状态的δ、θ 和α脑电功率谱均无显著变化。结论: 可卡因戒断所致睡眠障碍主要由于快、慢波睡眠间而非睡眠与觉醒间异动。急性戒断造成睡眠觉醒间转换异常,而睡眠结构失调则发生在亚急性和亚慢性戒断期间。     

失眠症患者状态-特质焦虑与睡眠结构的关系

目的:探讨失眠症患者睡眠结构改变与状态焦虑和特质焦虑的关系.方法:对31例失眠症患者和20例正常对照者进行状态-特质焦虑问卷调查和整夜多导睡眠图描记,失眠症组于症状缓解出院后3~4月回访时重复检查.结果:(1)在睡眠结构上,与对照组相比,失眠症组呈现睡眠时间减少[(333.71±84.33)min vs.(403.65±19.29)min]、睡眠效率下降[(70.41±17.35) % vs.(83.45±4.42) %]、睡眠潜伏期[(39.48±24.24) min vs.(19.65±8.57) min]和快速眼动睡眠潜伏期延长[(106.60±42.89) min vs.(86.80±12.25) min],S_1睡眠时间比例增加[( 25.36±14.22) %vs.(8.86±1.77) %]、觉醒次数增多[(4.45±2.51) vs.(1.75±1.07)].S_(3+4)睡眠[(7.38±9.70)% vs.(13.78±4.24)%]和快速眼动睡眠时间比例[( 14.54±5.61) %vs.(19.18±2.14) %]减少 (Ps<0.05).(2)在状态-特质焦虑问卷评分上,失眠症组状态焦虑[(47.94 ±8.96) vs.(39.15±4.51)]和特质焦虑[(49.94 ±8.90) vs.(42.05±7.13)]得分均高于对照组(Ps<0.05).状态焦虑与睡眠潜伏期、快眼动睡眠潜伏期、觉醒次数和S_1睡眠时间比例均呈正相关(r=0.25~0.44,Ps<0.05),而与快眼动睡眠时间比例呈负相关(r=-0.41,P<0.01);特质焦虑与睡眠潜伏期和觉醒次数正相关(r=0.37,0.29;均Ps<0.05).(3)回访时患者睡眠结构改善,状态焦虑得分下降,特质焦虑无明显变化.结论:失眠症患者有明显的睡眠结构改变和较高的状态焦虑和特质焦虑,其睡眠结构改变与状态焦虑和特质焦虑相关.     

孤独症谱系障碍儿童的睡眠行为

目的:探讨学前期和学龄期孤独症谱系障碍(autism spectrum disorders,ASD)儿童的睡眠行为的特点和差异。方法:选取符合美国精神障碍诊断与统计手册第4版(DSM-IV)诊断标准的ASD儿童84名和年龄性别匹配的正常儿童91名,使用儿童睡眠习惯问卷(CSHQ)和一周睡眠日记,由儿童主要照顾者记录儿童的睡眠情况。依据CSHQ总分大于41分为睡眠不良,以具体条目中睡眠行为发生频率超过2晚/周的标准界定睡眠行为问题,分3～5岁和6～12岁两个年龄段比较ASD与对照组儿童在睡眠行为和习惯上的差异。结果:3～5岁ASD组儿童CSHQ的睡眠潜伏期[(2.1±0.8)vs.(1.6±0.7)]、睡眠持续情况[(5.4±1.7)vs.(4.8±1.3)]得分高于对照组,入睡困难(77.6%vs.49.0%)、睡眠量不足(63.3%vs.42.9%)、夜醒哭闹(34.7%vs.12.2%)及日间疲乏(36.7%vs.10.2%)的比例较对照组高(均P0.05)。6～12岁ASD儿童平时睡眠总时长短于对照组[(8.68±0.76)h vs.(9.33±1.00)h],CSHQ的入睡抵触[(10.1±2.8)vs.(8.6±2.5)]、睡眠潜伏期[(1.7±0.7)vs.(1.4±0.6)]与睡眠焦虑[(5.4±2.0)vs.(4.5±1.9)]得分高于对照组,入睡困难(54.3%vs.31.0%)、睡眠量不足(60.0%vs.35.7%)、与父母同睡(65.7%vs.38.1%)、入睡需陪伴(68.6%vs.35.7%)的比例较对照组高(均P0.05)。结论:ASD儿童普遍存在睡眠总量少、入睡困难等问题,学龄前期以夜醒后哭闹和白天疲倦较为突出,而学龄期则以睡眠焦虑较为明显。     

澳门特别行政区初三学生的睡眠质量、睡眠模式与抑郁、焦虑情绪

目的:了解澳门特别行政区初三年级学生的睡眠质量、模式与抑郁、焦虑情绪的关系。方法:抽取澳门535名初中三年级学生,用匹兹堡睡眠质量指数量表(PSQI)评估睡眠质量,爱泼沃斯思睡量表(ESS)以及清晨型和夜晚型量表(MEQ)调查白天思睡与睡眠模式,用贝克抑郁量表(BDI)、状态-特质焦虑量表(STAI)调查抑郁、焦虑状况。结果:PSQI和ESS得分分别为(5.2±2.6)和(8.4±4.7),女生PSQI[(5.5±2.5)vs.(4.8±2.6)]和ESS[(8.9±4.6)vs.(8.0±4.8)]得分高于男生(均P0.05)。MEQ平均得分(13.3±3.1),女生得分低于男生[(12.8±3.0)vs.(13.7±3.2),P0.01]。学生周末和假日的总睡眠时间长于平日总睡眠时间[(608±106)min,(605±109)min vs.(457±75)min],女生周末[(628±110)min vs.(590±97)min]和假期[(631±109)min vs.(581±103)min]平均睡眠时间长于男生(均P0.01)。BDI和STAI得分分别为(13.5±10.3)、(78.9±17)。睡眠质量差和白天思睡者MEQ得分、上学日睡眠时间低于睡眠质量好和无白天思睡者MEQ得分,而睡眠质量差和白天思睡者BDI得分高于睡眠质量好和无白天思睡者BDI得分(均P0.05)。PSQI分别与ESS、BDI,以及STAI中的TAI分呈正相关(r=0.27、0.37、0.12,均P0.05),而与M EQ和上学日总睡眠时间呈负相关(r=-0.30、-0.30,均P0.05)。结论:睡眠质量差和白天思睡在澳门初三学生中较为普遍,他们在上学日的平均睡眠时间不足,但在周末和假日则延长睡眠时间以作补充,其中女生更易出现上述睡眠模式。大部分学生有轻度抑郁,睡眠质量差可能与其抑郁、焦虑状况相关。     

中缝背核在睡眠-觉醒中的作用

中缝背核(DRN)是调控睡眠-觉醒的重要核团,在脑内有着广泛的神经投射区域。DRN位于中脑导水管腹侧,主要由5-羟色胺(5-HT)、γ-氨基丁酸(GABA)、多巴胺(DA)和谷氨酸(Glu)能4类神经元构成。本文主要介绍了DRN的各类神经元在睡眠-觉醒中相关作用的最新研究进展。     

氮硝基左旋精氨酸对烟雾吸入性损伤大鼠肺保护作用的研究

目的探讨氮硝基左旋精氨酸对烟雾吸入性损伤大鼠肺组织的保护作用。方法雄性Sprague-Dawle大鼠60只采用随机数字表法分为4组,空白组6只,余下分为生理盐水组、低剂量组和高剂量组,每组设6h、24h、48h三个时相点,各时相点6只。空白组不予任何处理,其余3组大鼠制作烟雾吸入性损伤模型,生理盐水组、低剂量组和高剂量组于伤后分别腹腔注射等容量的生理盐水、浓度为10mg/kg的氮硝基左旋精氨酸和浓度为20mg/kg的氮硝基左旋精氨酸。注射30min后将每只大鼠股动脉取血5mL,离心后检测血清白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)含量,活杀后取部分左肺匀浆后检测丙二醛(MDA)、髓过氧化物酶(MPO)及超氧化物歧化酶(SOD)含量,取部分右肺经4%甲醛溶液固定后做病理苏木精-伊红染色切片光镜观察。结果低剂量组48h与同时相点生理盐水组相比,TNF-α[(179.51±8.67)ng/L vs (231.39±9.98)ng/L],IL-6[(289.01±31.84)pg/mL vs(398.67±32.93)pg/mL],MDA[(4.37±0.62)nmol/mg vs (4.41±0.35)nmol/mg],MPO[(41.39±1.49)U/g vs (50.18±1.72)U/g]降低,差异有高度统计学意义(P<0.01),SOD[(93.82±5.69)U/mg vs (88.46±5.48)U/mg]和IL-10[(110.33±4.21)ng/L vs (108.85±5.47)ng/L]升高,差异有高度统计学意义(P<0.01)。高剂量组比低剂量组差异更显著。病理切片显示致伤后6h低剂量组和高剂量组大鼠相较生理盐水组肺组织炎细胞浸润减少,肺泡萎陷程度减轻,其中高剂量组比低剂量组改善更明显。结论氮硝基左旋精氨酸可减轻大鼠吸入性损伤后肺组织中炎性反应及过氧化反应,从而减轻肺损伤的程度。     

糖皮质激素对类风湿关节炎炎性因子改变及效果的观察

目的：分析糖皮质激素对类风湿关节炎炎性因子改变及效果。方法：选取我院2014年8月至2015年8月门诊及住院就诊的80例类风湿关节炎患者,依据抽签法分成对照组与观察组,每组40例,对照组采取常规治疗,观察组基于对照组联合糖皮质激素治疗,对比分析两组治疗后炎性因子、RF、ESR、晨僵、关节肿胀数及关节压痛数、DAS评分及VAS评分变化、治疗有效率与不良反应。结果：治疗后,观察组炎性因子TNF-α低于对照组[(31.23±8.74) vs.(36.46±9.12) pg/mL],IL-6低于对照组[(2.62±0.31) vs.(3.67±0.36) pg/L],CRP低于对照组[(15.26±1.03) vs.(17.38±1.10) mg/L],比较有显著差异(P<0.05);观察组RF低于对照组[(15.34±1.21) vs.(20.25±1.24) U/mL],ESR低于对照组[(24.36±1.57) vs.(28.95±1.60) mm/h],晨僵少于对照组[(16.73±1.28) vs.(18.97±1.34)],关节肿胀数低于对照组[(47.28±0.40) vs.(6.73±0.45)],关节压痛数低于对照组[(6.18±0.52) vs.(9.36±1.05) min],比较差异显著(P<0.05);观察组DAS28低于对照组[(1.93±0.20) vs.(2.18±0.26)分],VAS低于对照组[(2.23±0.25) vs.(3.07±0.12)分],比较差异明显(P<0.05);治疗有效率95.00%高于对照组80.00%(P<0.05),观察组总不良反应率25.00%高于对照组20.00%,但无统计学意义(P>0.05)。结论：类风湿关节炎运用糖皮质激素治疗安全性高,可有效降低炎性因子水平,改善患者临床症状,促进身心恢复。     

睡眠剥夺影响执行控制的功能磁共振成像研究

目的: 探讨完全睡眠剥夺(total sleep deprivation,TSD)对大脑执行控制功能的影响.方法: 采用自身前后对照设计.以13名健康男性大学生作为被试,进行两次Go/No-go测验,同时进行功能磁共振成像(functional magnetic resonance imaging,fMRI)扫描,第一次在正常睡眠后12小时完成,第2次间隔3周在睡眠剥夺36小时后完成.结果: 与睡眠后的Co/No-go测试成绩相比,睡眠剥夺后被试的正确击中率下降[(0.99±0.01)vs.(0.97±0.04),P＜0.05)],错误反应率增高[(0.04±0.04)vs.(0.10±0.08),P＜0.05].fMRI结果显示前扣带回皮质活动降低[(-0.391±0.003)vs.0;P＜0.05],前额叶皮质活动明显增强[(0.653±0.003)vs.0;P＜0.05].结论: 睡眠剥夺36小时导致执行抑制功能的显著下降,前额叶皮质出现功能代偿是维持认知作业的重要特征.     

白介素-10的新型抑制剂AS101对大鼠睡眠觉醒周期的影响

目的:研究不同剂量AS101[白介素-10(IL-10)的新型抑制剂]对大鼠睡眠觉醒周期的影响.方法:采用脑立体定位、脑电图及肌电图记录方法研究AS101对睡眠的影响.结果:与注射pH7.4的缓冲液组大鼠比较,夜间小剂量组AS101对大鼠睡眠觉醒周期没有影响;而白天小剂量组AS101增加大鼠慢波睡眠时间,从(276.28±35.73)min增加到(308.38±30.68)min,减少觉醒时间,从(165.00±35.12)min,减少到(134.36±24.47)min;白天大剂量组AS101明显增加大鼠慢波睡眠时间,从(272.28±35.16)min 增加到(302.98±28.11)min, 而对快速眼动睡眠没有影响.结论:AS101可增加大鼠慢波睡眠时间,有调节睡眠觉醒周期的作用.     

Interleukin-8 promotes non-rapid eye movement sleep in rabbits and rats

Interleukin-8 (IL-8) is a cytokine found in the brain. In this study, the ability of IL-8 to induce sleep in rabbits and rats was investigated. Twenty-seven Sprague-Dawley rats and 16 male New Zealand White rabbits were provided electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular cannula. The animals were injected intracerebroventricularly (i.c.v.) with pyrogen-free saline and, one of the following doses of IL-8 on a separate day: 1.25 or 12.5 ng in rabbits and 10, 50, or 100 ng in rats. EEG, brain temperature, and motor activity were recorded for 23 h after the i.c.v. injections. IL-8 increased time spent in non-rapid eye movement sleep (NREMS) without affecting rapid eye movement sleep (REMS). In rabbits, both doses of IL-8 promoted NREMS. In rats, the 10 and 50 ng doses of IL-8 failed to affect sleep, but the 100 ng dose of IL-8 enhanced NREMS. EEG slow-wave activity during NREMS was increased after the high dose of IL-8 in rabbits. IL-8 also induced fever in rabbits but not rats. Heat inactivated IL-8 did not alter any of the parameters measured. Current results support the notion that the brain cytokine network plays a role in sleep regulation.     

Selective 5HT2A and 5HT6 receptor antagonists promote sleep in rats

STUDY OBJECTIVES: Serotonin (5-HT) has long been implicated in the control of sleep and wakefulness. This study evaluated the hypnotic efficacy of the 5-HT6 antagonist RO4368554 (RO) and the 5-HT2A receptor antagonist MDL100907 (MDL) relative to zolpidem. DESIGN: A randomized, repeated-measures design was utilized in which Wistar rats received intraperitoneal injections of RO (1.0, 3.0, and 10 mg/kg), MDL (0.1, 1.0 and 3.0 mg/kg), zolpidem (10 mg/kg), or vehicle in the middle of the dark (active) period. Electroencephalogram, electromyogram, body temperature (Tb) and locomotor activity were analyzed for 6 hours after injection. MEASUREMENTS AND RESULTS: RO, MDL, and zolpidem all produced significant increases in sleep and decreases in waking, compared with vehicle control. All 3 doses of MDL produced more consolidated sleep, increased non-rapid eye movement sleep (NREM) sleep, and increased electroencephalographic delta power during NREM sleep. The highest dose of RO (10.0 mg/kg) produced significant increases in sleep and decreases in waking during hour 2 following dosing. These increases in sleep duration were associated with greater delta power during NREM sleep. ZO Zolpidem induced sleep with the shortest latency and significantly increased NREM sleep and delta power but also suppressed rapid eye movement sleep sleep; in contrast, neither RO nor MDL affected rapid eye movement sleep. Whereas RO did not affect Tb, both zolpidem and MDL reduced Tb relative to vehicle-injected controls. CONCLUSIONS: These results support a role for 5-HT2A receptor modulation in NREM sleep and suggest a previously unrecognized role for 5-HT6 receptors in sleep-wake regulation.     

Reactive oxygen products in heterologous anti-glomerular basement membrane nephritis in rats.

The effect of ''scavengers'' of reactive oxygen products (ROPs) was studied in the heterologous phase of anti-glomerular basement (anti-GBM) nephritis induced in rats. Glomerulonephritis was induced by the intravenous administration of sheep anti-GBM antibody (5 mg/100 g) to rats on day 0. The intraperitoneal administration of superoxide dismutase (SOD) 30 mg/kg/day or 150 mg/kg/day leads to a significant reduction in proteinuria on day 1 and also on day 3 in animals given SOD 30 mg/kg/day. Proteinuria was not significantly reduced by the intraperitoneal administration of inactivated SOD (150 mg/kg/day). In rats given polyethylene glycol coupled catalase (PEG-catalase) intraperitoneally at a dose of 10,000 iu/kg/day and 100,000 iu/kg/day proteinuria was lower than in rats with unmodified anti-GBM nephritis. These differences were significant on day 1 (P less than 0.05) in rats given PEG-catalase 100,000 iu/kg/day and on days 3 and 5 in rats treated with either dose of PEG-catalase (P less than 0.01). These data suggest a role for superoxide anion and hydrogen peroxide, or a product of their interaction such as hydroxyl radical, in glomerular injury induced by anti-GBM antibody.     

Reactive oxygen products in heterologous anti-glomerular basement membrane nephritis in rats

The effect of 'scavengers' of reactive oxygen products (ROPs) was studied in the heterologous phase of anti-glomerular basement (anti-GBM) nephritis induced in rats. Glomerulonephritis was induced by the intravenous administration of sheep anti-GBM antibody (5 mg/100 g) to rats on day 0. The intraperitoneal administration of superoxide dismutase (SOD) 30 mg/kg/day or 150 mg/kg/day leads to a significant reduction in proteinuria on day 1 and also on day 3 in animals given SOD 30 mg/kg/day. Proteinuria was not significantly reduced by the intraperitoneal administration of inactivated SOD (150 mg/kg/day). In rats given polyethylene glycol coupled catalase (PEG-catalase) intraperitoneally at a dose of 10,000 iu/kg/day and 100,000 iu/kg/day proteinuria was lower than in rats with unmodified anti-GBM nephritis. These differences were significant on day 1 (P less than 0.05) in rats given PEG-catalase 100,000 iu/kg/day and on days 3 and 5 in rats treated with either dose of PEG-catalase (P less than 0.01). These data suggest a role for superoxide anion and hydrogen peroxide, or a product of their interaction such as hydroxyl radical, in glomerular injury induced by anti-GBM antibody.     

The in vivo and in vitro effects of caffeine on rat immune cells activities: B, T and NK cells

The effect of caffeine (naturally occurring plant methylxanthine) on immunological cell activities in Sprague-Dawley rat both in vivo and in vitro was studied. A cytotoxic assay was done to study natural killer (NK) cells and a proliferation assay was performed for T and B cell activities. Three different doses of caffeine i.e., 2, 6 and 18 mg/kg/day were administered chronically to Sprague-Dawley rats to assess the effects in vivo. Both NK cell cytotoxicity and B cell proliferative response to pokeweed mitogen (PWM) showed significant decreases (P less than 0.05) in rats treated with 6 mg/kg/day, whereas the T cell proliferative response to phytohemagglutinin-P (PHA-P) was significantly increased (P less than 0.05) in the rats treated with 18 mg/kg/day. In vitro, caffeine significantly decreases (P less than 0.05) B and T cell proliferative responses to PWM and PHA-P at added caffeine concentrations of 10, 20 and 40 micrograms/ml. However, no effect was observed on NK cells activity. Furthermore, in vitro, a broader dose range of caffeine (1, 10, 100 and 1,000 micrograms/ml) exhibited dose-dependent inhibition of both B and T cell proliferative responses.     

The effects of soy extract on the uterus of castrated adult rats

OBJECTIVE: The aim of this study was to evaluate the effects of different doses of a standardized soy extract on the uterus of castrated rats. METHODS: Fifty-six adult castrated female Wistar rats were randomly divided into seven groups (eight animals in each) that received: GI--drug vehicle (propylene glycol); GII--soy extract 10mg/kg per day; GIII--soy extract 50mg/kg per day; GIV--soy extract 100mg/kg per day; GV--soy extract 300mg/kg per day; GVI--soy extract 600mg/kg per day; GVII-conjugated equine estrogens (CEE) 200microg/kg per day. After 21 days of treatment, all animals were sacrificed and fragments of the uterine horns were immediately removed, fixed in 10% formaldehyde and submitted to routine histological techniques for morphometric study. The endometrial cell proliferation index was determined with the PCNA antibody PC-10 and expressed as the percentuals of the PCNA-positive nuclei relative to the total countings. Other fragments were immediately frozen in liquid nitrogen for RNA extraction and VEGF analysis using RT-PCR technique. RESULTS: The minimal dose of soy extract that produced a significant increase of the morphometric parameters was 100mg/kg (GIV). The maximum effects on endometrial and myometrial morphometry were detected in the groups treated with 300 and 600mg/kg of soy extract (groups V and VI) and CEE (GVII). The expression of PCNA in the endometrial epithelium and stroma was increased by treatment with 100-600mg/kg per day of soy extract (groups IV-VI) or with CCE (group VII). Doses equal to or higher than 50mg/kg of soy extract (groups III-VI) and CEE stimulated the expression of VEGF. CONCLUSION: The treatment of adult castrated rats during 21 days with doses of 100mg/kg per day or higher of soy extract may determine significant proliferation in the endometrium and myometrium.     

Sleep deficits in rats after NMDA receptor blockade.

N-Methyl-D-aspartate (NMDA) receptor blockade disrupts a variety of functions associated with neural plasticity, including acquisition of learned responses and long-term potentiation. Deficits in memory are significantly correlated with deficits in measures of paradoxical sleep in several amnesic populations. The present experiment therefore assessed whether NPC 12626, a competitive NMDA receptor antagonist, also disrupts sleep. NPC 12626 (1, 10, 50, and 100 mg/kg) or saline was administered to Sprague-Dawley rats 30 min prior to 3-h daytime recording periods. Paradoxical sleep was selectively impaired at all but the highest dose, which prevented all sleep during the recording period. Some deficits in nonparadoxical sleep first appeared at the 10 mg/kg dose but did not became prominent until the 50 mg/kg dose. The results thus show that NPC 12626 impairs sleep states in rats and demonstrate that paradoxical sleep is particularly susceptible to the effects of NMDA receptor blockade. These findings, along with previous evidence that NMDA antagonists impair waking measures of arousal, provide evidence that all sleep-wake states are impaired by NMDA receptor blockade. More generally, the results suggest that some brain mechanisms underlying sleep and memory may share common elements.     

Assessing sleepiness in the rat: a multiple sleep latencies test compared to polysomnographic measures of sleepiness

Sleepiness following 6 h of sleep deprivation (SD) was evaluated with a rat multiple sleep latencies test (rMSLT), and the findings were compared to conventional polysomnographic measures of sleepiness. The 6 h of SD was produced by automated activity wheels, and was terminated at either the end of the light period or at the beginning of the dark period. The rMSLT consisted of 5 min wakefulness induced by sensory stimulation followed by 25 min of freedom to sleep. This procedure was repeated every 30 min for 3 h and was designed to minimize the amount of sleep lost due to the testing procedure. In separate rats, 6 h SD was followed by undisturbed recovery, allowing evaluation of conventional polysomnographic measures of sleepiness. Sleep onset latencies were reduced following SD, with recovery in the light (baseline = 8 min, 3 s versus post-SD = 1 min, 17 s) and dark period (baseline = 14 min, 17 s versus 7 min, 7 s). Sleep onset latencies were not altered by varying the duration criterion for the first sleep bout (i.e., sleep bout length criteria of 10, 20, 30, or 60 s were compared). Polysomnographic variables (non-rapid eye movement sleep episode duration, delta power, and number of awakenings) also provided reliable indirect measures of sleepiness, regardless of whether the recovery sleep occurred in the light or dark period. Evaluation of effect size indicated that the rMSLT was a strong measure of sleepiness, and was influenced by homeostatic, circadian, and illumination factors. The rMSLT provided a simple, objective, robust and direct measure of sleepiness that was as effective as conventional polysomnographic measures of sleepiness.