睡眠剥夺对小鼠脑内细胞型朊蛋白表达水平的影响及可能的意义

目的 探讨小鼠正常昼夜节律下以及睡眠剥夺后大脑海马组织细胞型朊蛋白(PrP^C)和β-淀粉样前体蛋白(Aβ)表达水平的变化及PrP^C在睡眠剥夺诱导的认知损害中发挥的作用。方法 成年C57BL/6小鼠置于光照和黑暗交替环境中饲养2周后分别在开灯后4、8、12、16、20、24 h等6个时间点处死小鼠,每个时间点各8只,分别取海马、皮层2个部位的组织样本,采用酶联免疫吸附法检测PrP^C和Aβ的表达水平。成年小鼠按体重大小排序,完全随机分成3组,分别为正常对照组、环境对照组、睡眠剥夺组,采用改良水平台法对小鼠进行72h快速眼动睡眠剥夺,断头处死小鼠获取海马,分别采用Western Blot法和酶联免疫吸附法检测PrP^C和Aβ的表达水平变化。Halberg余弦分析PrP^C和Aβ在海马与皮层的昼夜节律变化特征。结果 单余弦分析显示PrP^C在皮层具有昼夜节律性(F=11.22,P<0.05)。Aβ在海马具有昼夜节律性(F=26.72,P<0.05); 睡眠剥夺后睡眠剥夺组海马PrP^C的表达水平(0.22±0.05)较正常对照组(0.64±0.16)和环境对照组(0.58±0.09)明显下调(F=4.366,P<0.05),睡眠剥夺组Aβ的表达水平(13.03±0.71)较正常对照组(8.22±0.8)和环境对照组(8.6±0.57)明显上调(F=14.511,P<0.05)。结论 正常小鼠大脑PrP^C和Aβ具有昼夜节律特征,快速眼动睡眠剥夺后PrP^C的表达水平下调,而Aβ表达水平上调,且这可能是睡眠剥夺后认知功能障碍的潜在机制之一。     

快速眼动睡眠剥夺后大鼠脑内神经元骨架蛋白及超微结构的变化

目的探讨经历不同时间快速眼动（REM）睡眠剥夺对大鼠皮质及海马各区神经元形态结构的影响。方法选择微管相关蛋白（MAP2）和神经丝（NF）作为正常神经元结构的标识物，利用免疫组织化学法和Western blot技术观察REM睡眠剥夺1、3、5、7 d4个时间点大鼠皮质及海马MAP2和NF表达的时空变化规律。同时运用电镜技术观察睡眠剥夺后神经元超微结构的变化。我们的实验是用改良的多平台睡眠剥夺模型进行REM睡眠剥夺，结合免疫组织化学染色技术和蛋白质电泳以及电镜超微结构分析。结果REM睡眠剥夺后5d大鼠皮质、海马CA1及齿状回神经元结构蛋白MAP2和NF表达较对照组明显减少（P〈0．05）；电镜神经元核仁偏位，胞质中出现少量肿胀的线粒体和内质网；部分神经轴突的髓鞘溶解与浓集。环境对照组、REM睡眠剥夺5d和7d组，皮质中超微结构改变的神经元所占比例分别为1．2％、3．6％和5．8％。结论REM睡眠剥夺能够导致大鼠脑内神经元的超微结构发生异常变化。     

重视睡眠剥夺导致认知功能障碍机制的脑功能成像研究

睡眠的不同阶段具有不同的生理功能,各种原因诱发的睡眠剥夺(SD)或失眠都能损害相关睡眠期的生理功能。已知睡眠剥夺或失眠与神经系统变性疾病、心脑血管疾病、内分泌系统疾病及精神疾病等密切相关,因此引起了各专     

大鼠正常睡眠和睡眠剥夺后食欲素原 mRNA的表达

目的研究正常睡眠和睡眠剥夺后大鼠下丘脑和大脑皮质食欲素原mRNA的表达。方法用转筒法剥夺大鼠的睡眠,用逆转录聚合酶链反应(RT PCR)检测正常睡眠和不同剥夺睡眠时间大鼠下丘脑和大脑皮质食欲素原mRNA的表达。结果大鼠下丘脑的食欲素原mRNA昼夜有明显变化(光暗期6 00的0 406±0 012和光亮期18 00的0 835±0 045相比,P<0 01)。而在大脑皮质没有明显的昼夜变化。正常大鼠下丘脑的食欲素原mRNA表达要高于大脑皮质;短时间的睡眠剥夺不影响下丘脑和大脑皮质食欲素原mRNA的表达(对照组0 406±0 012与剥夺4h0 398±0 034相比,P>0 05),而睡眠剥夺8h后下丘脑和大脑皮质食欲素原mRNA的表达明显增加(对照组0 406±0 012与剥夺8h0 518±0 043、剥夺12h0 636±0 047和剥夺24h0 827±0 042,P<0 01)。结论食欲素与睡眠之间有密切的关系,正常睡眠的控制有赖于下丘脑的食欲素的调节。     

轻度认知障碍患者睡眠障碍的研究进展

<正>轻度认知障碍(Mild Cognitive Impairment,MCI)常常伴发多种睡眠-觉醒障碍疾病,包括失眠、睡眠相关的呼吸障碍、REM期睡眠行为障碍、昼夜节律失调性睡眠-觉醒障碍、日间过度思睡、不宁腿综合征。MCI患者的睡眠障碍会影响患者的生活质量、加重认知功能障碍、增加照料者负担。对MCI的睡眠-觉醒障碍应该进行常规和全面的评估,了解MCI睡眠障碍类型和影响因素,才能给予患者个体化的治     

睡眠剥夺大鼠大脑皮层和海马nNOS表达的改变在其学习记忆损伤中的作用

目的观察睡眠剥夺（SD）后,大鼠学习记忆能力及大脑皮层和海马神经元型一氧化氮合酶（nNOS）蛋白表达的变化。方法采用小平台水环境法建立大鼠SD模型。观察大鼠经过不同时间SD后,各组“Y”迷宫成绩及大脑皮层和海马nNOS阳性神经元的变化情况。结果（1）“Y”迷宫实验：3组SD组的迷宫成绩较正常笼养对照组（CC）分别下降了24．3％、17．6％和41．9％（P〈0．01）。（2）nNOS阳性神经元数目：在皮层,SDld组较CC组增加了8．7％（P〈0．01）,SD2d组和SD3d组较CC组则减少了9．0％和16．0％（P〈0．01）;在海马CA。区,3个SD组较CC组分别减少了9．4％、16．0％和22．0％（P〈0．01）。结论SD可能通过改变大鼠大脑皮层和海马CA．区nNOS蛋白的表达来损害大鼠学习记忆能力。     

睡眠剥夺及睡眠恢复后大鼠中缝核群星形胶质细胞的反应及其与神经元的关系

目的探索睡眠剥夺及睡眠恢复后大鼠脑干中缝核群星形胶质细胞的反应及其与神经元的关系。方法采用小平台水环境法建立大鼠睡眠剥夺模型,20只大鼠分为睡眠剥夺12h组,睡眠剥夺12h恢复睡眠3h组及大平台对照组和正常单独饲养组,每组5只,用免疫组化的方法测量glial fibrillary acidic protein(GFAP)和Fosprotein在脑干中缝核群的表达。结果睡眠剥夺后GFAP-like immunoreaction(LI)星形胶质细胞和FosLI神经元在中缝核群各核有明显表达,睡眠恢复后表达明显减少,两者的变化趋势基本一致。结论睡眠剥夺影响GFAPLI星形胶质细胞和FosLI神经元的表达,提示星形胶质细胞和神经元可能共同参与睡眠调节。     

睡眠剥夺对大鼠海马和皮质IL-1β蛋白表达的影响

目的:研究完全睡眠剥夺对大鼠海马和皮质IL-1β蛋白表达的影响。方法:将大鼠放入1转/分钟转笼中,制作经历不同持续时间的完全睡眠剥夺(TSD)模型。30只大鼠随机分为5组:对照组(正常对照CC组,环境对照TC组)和睡眠剥夺组[TSD6h组,TSD1d组,TSD3d组(n=6只)]。采用免疫组化方法检测大鼠海马和皮质IL-1β蛋白表达。结果:IL-1β阳性细胞大多在细胞浆,胞核内也有表达;主要分布在海马CA3、CA1及齿状回细胞核和细胞浆,在大脑皮质分布于各层。结论:完全睡眠剥夺大鼠海马和皮质IL-1β蛋白表达增高,且随时间的延长而逐趋明显。睡眠短期剥夺,IL-1β蛋白表达增高可能对脑细胞具有应激性保护作用,而长期剥夺后IL-1β持续增高可能对神经元有损伤作用。     

睡眠剥夺小鼠海马中BDNF、IL-4变化的研究

目的探究睡眠剥夺过程中小鼠海马组织内脑源性神经营养因子(brain derived neurotrophic factor,BDNF)、白细胞介素4(Interleukin-4,IL-4)的动态变化及相关性,从而为睡眠剥夺对海马学习记忆功能的影响提供可能的理论依据。方法 (1) 6～8周龄C57BL/6J雄性小鼠随机分为正常对照组(Cage control,CC)、快速眼球运动(REM)睡眠剥夺1 d组(REM sleep deprivation 1 day,SD 1 d)、REM睡眠剥夺2 d组(SD 2 d)、REM睡眠剥夺3 d组(SD 3 d),每组12只小鼠。CC组同笼饲养1 w后于9:00AM灌注处死,SD 1 d组、SD 2 d组、SD 3 d组经睡眠剥夺1 d、2 d和3 d后均于9:00AM灌注处死。(2)采用ELISA方法观察各组小鼠海马组织中BDNF、IL-4的表达水平。结果 (1) ELISA显示SD 1 d组小鼠海马中BDNF、IL-4较CC组表达水平升高,差异具有统计学意义(P值分别为0. 029、0. 001); SD 2 d组BDNF、IL-4较CC组表达无明显差异(P值分别为 0. 5、0. 13); SD 3 d组BDNF、IL-4较CC组表达水平明显降低,差异具有统计学意义(P值均为0. 001)。(2) Pearson相关性分析显示睡眠剥夺过程中小鼠海马中IL-4、BDNF蛋白表达变化呈正相关性,P 0. 001,相关系数r=0. 863。结论睡眠剥夺后BDNF、IL-4表达量的变化可能是睡眠剥夺后造成神经损伤的可能机制之一。     

睡眠剥夺影响数字记忆的功能磁共振成像研究

研究背景长时间连续作业易导致大脑疲劳,已有证据显示脑疲劳对作业者认知功能和行为反应能力具有严重损害作用,因此揭示连续作业和睡眠剥夺对认知功能影响的机制,有助于对抗连续作业所致疲劳,提高连续作业能力。本研究通过分析睡眠剥夺前后功能磁共振成像(fMRI)特点,探讨睡眠剥夺影响学习记忆的神经机制。方法共6例健康男性志愿者接受48h睡眠剥夺,采用组块设计方法评价睡眠剥夺前后数字记忆功能变化,fMRI比较数字记忆编码、维持和提取阶段各脑区的激活特点。结果睡眠剥夺48h,受试者对4～7个0～9数字记忆的错误率并未增加(均P>0.05);对4～6个0～9数字记忆的反应时间与睡眠剥夺前无明显差异(均P>0.05),仅7个0～9数字记忆的反应时间增加(P=0.005)。睡眠剥夺后激活减弱的脑区在数字记忆试验编码阶段为左侧海马旁回Brodmann30区、颞上回Brodmann42区、岛叶Brodmann41区和额叶Brodmann6区;在维持阶段分别为左侧颞上回Brodmann38区、颞中回Brodmann21区、海马旁回和杏仁核Brodmann30区、额中回Brodmann47区、豆状核和丘脑,以及右侧豆状核、左侧扣带后回Brodmann30区、右侧扣带后回Brodmann30区、双侧扣带回Brodmann24区、双侧额中回和额内侧回Brodmann6区;提取阶段包括双侧海马、右侧杏仁核和顶下小叶Brodmann40区、左侧楔前叶Brodmann19区和丘脑。结论在数字记忆的不同阶段,机体通过激活不同的脑区来维持清醒状态,48h睡眠剥夺后参与数字记忆的大脑皮质及皮质下结构广泛受损。     

Effect of repetitive transcranial magnetic stimulation on the cognitive impairment induced by sleep deprivation: a randomized trial

ObjectiveCurrently, an efficient method for improving cognitive impairment due to sleep deprivation (SD) is lacking. The aim of this study is to evaluate the effect of high-frequency repetitive transcranial magnetic stimulation (rTMS) during SD on reversing the adverse effects of SD.MethodsA total of 66 healthy people were randomized into the rTMS group and sham group. Both groups were deprived of sleep for 24 h. During SD, participants were asked to complete several cognitive tasks and underwent mood assessments. Saliva cortisol levels, plasma concentrations of brain-derived neurotrophic factor (BDNF), precursor BDNF (proBDNF), and tissue-type plasminogen activator (tPA), and frontal blood activation were detected before and after SD. The rTMS group received real rTMS stimulation for 2 sessions of 10 Hz rTMS (40 trains of 50 pulses with a 20-second intertrain interval) to the left dorsolateral prefrontal cortex and the sham group received sham stimulation during SD.ResultsTwenty-four hours of SD induced a reduced accuracy in the n-back task, increases in both anxiety and depression, increased cortisol levels, decreased frontal blood activation and decreased BDNF levels in healthy people. Notably, rTMS improved the hyperactivity of the hypothalamic-pituitary-adrenal axis and decreased frontal blood activation induced by SD, and reduced the consumption of plasma proBDNF.ConclusionsTwenty-four hours of SD induced a cognitive impairment. The administration of high-frequency rTMS during sleep deprivation exerted positive effects on HPA axis and frontal activation and might help alleviate cognitive impairment in the long term.     

Modafinil reduces microsleep during partial sleep deprivation in depressed patients

Objective

Sleep deprivation (SD) can induce a prompt decrease in depressive symptoms within 24 h. Following the recovery night, however, a relapse into depression occurs in most patients. Recovery sleep, naps and even very short episodes of sleep (microsleep; MS) during SD have been shown to provoke a rapid relapse into depression. This study tested the hypothesis that modafinil reduces MS during SD and stabilizes the treatment response to PSD compared to placebo.

Methods

A total of 28 patients (13 men, 15 women; age 45.1 ± 12.1 years) with a major depressive episode and a cumulative daytime microsleep of five or more minutes were investigated using a double-blind placebo-controlled study design. All patients were treated with a stable mirtazapine monotherapy. A partial SD (PSD) was performed after one week. Additional morning treatment with modafinil vs. placebo started during PSD and was maintained over two weeks. Sleep-EEG and MS episodes were recorded with a portable EEG. Depression severity was assessed using the Hamilton Depression Rating Scale before, during and after PSD and at follow-ups after one and two weeks.

Results

Patients treated with modafinil showed significantly reduced microsleep during PSD (11.63 ± 15.99 min) compared to the placebo group (47.77 ± 65.31 min). This suppression of MS was not associated with the antidepressive effect of PSD.

Conclusions

Compared to placebo, modafinil was efficient in reducing daytime microsleep following partial sleep deprivation but did not enhance the antidepressive effects of PSD and did not stabilize antidepressive effects over two weeks.     

不同记忆测验识别轻度认知损害的差异

目的分析不同的记忆测验对于轻度认知损害（MCI）的识别力的差异。方法2004年5月至2006年5月就诊于本院神经内科记忆障碍门诊的被试共712例，除了客观记忆指标，其余要求均符合MCI入组标准的有329例。全部入组者完成听觉词语学习测验（AVLT）、逻辑记忆测验（LM）、Rey-Osterrieth复杂图形测验（CFT）及MMSE、画钟测验、五点测验、言语流畅性测验、Stroop色词测验、连线测验、临床痴呆评定量表。结果对于MCI的识别率AVLT-Ⅱ（51％）〉AVLT-Ⅰ（31％）〉CFT回忆（27％）〉LM-Ⅰ（21％）=LM-Ⅱ（21％）。AVLT-Ⅱ与LM-Ⅱ均〉划界分者，为主观认知缺损（SCI）组，占47％（155／329）；AVLT-Ⅱ与LM-Ⅱ均≤划界分者，为确定MCI组，占19％（63／329）；AVLT-Ⅱ与LM-Ⅱ不一致，其中AVLT-Ⅱ≤划界分而LM-Ⅱ〉划界分者，为分歧组，占32％（104／329）。通过对各领域神经心理测验结果和临床表现进行比较，分歧组明显不同于SCI组，而是接近于确定MCI组，也就是说，分歧组是认知功能损害相对较轻的MCI。结论不同的情景记忆测验对于MCI的识别能力存在巨大的差异。AVLT延迟回忆最敏感，可以作为MCI“记忆减退的客观证据”。     

快速眼球运动睡眠剥夺及γ-氨基丁酸能药物干预对大鼠认知功能的影响

目的 建立快速眼球运动(REM)睡眠剥夺和下丘脑穹隆周围核微量渗析大鼠模型,研究不同程度REM睡眠剥夺和恢复对SD大鼠认知功能、下丘脑泌素(Hcrt)能系统和γ-氨基丁酸(GABA)能系统的影响及其可能机制.方法 将雄性SD大鼠随机分为对照组和REM睡眠剥夺组,REM睡眠剥夺组又分非手术对照组(nonOP)、假手术对照组(Sham)、GABAA受体拈抗剂SR-95531组(SR)和GABA再摄取抑制剂NO-711组(NO).采用改良多平台水环境法(MMPM)建立REM睡眠剥夺SD大鼠模型,利用Morris水迷宫测定大鼠在不同程度REM睡眠剥夺对认知功能的影响变化,采用免疫荧光技术检测下丘脑Hcrt神经元数量形态和原癌基因(Fos)表达、下丘脑GABA的A型受体α1(GABAA Rα1)亚单位表达累积吸光度值;采用高效液相色谱仪(HPLC)测定下丘脑GABA和谷氨酸(Glu)含量.建立穹隆周围核微量渗析SD大鼠模型,观察GABAA受体拈抗剂SR-95531和GABA再摄取抑制剂NO-711对上述指标的影响.结果 REM睡眠剥夺导致nonOP组和Sham组SD大鼠认知功能下降、下丘脑外侧区Fos阳性细胞总数和Fos-Hcrt双阳性细胞(F+&H+)数量增加、下丘脑GABA含量和GABAA Rα1表达增加,且变化程度均与REM睡眠剥夺时间长短呈正相关.但上述指标的变化都能够在不同程度睡眠恢复后得以修正.NO组与对照组比较,睡眠剥夺期间认知功能下降、下丘脑外侧区Fos阳性细胞总数和F+&H+数量增加(F=9.56、12.14、10.12,P＜0.05),且增加程度均与REM睡眠剥夺时间长短呈正相关;但睡眠恢复后差异无统计学意义.SR组与对照组比较,睡眠剥夺期间差异无统计学意义,但睡眠恢复期间认知功能下降、下丘脑外侧区Fos阳性细胞总数和F+&H+数量增加(F=12.03、11.38、8.36,均P＜0.05).SR组GABA含量和GABAA Rα1表达在全部5个时间点均明显增加(F=11.36、14.67,均P＜0.05),而NO组仅在SD 5d的GABAA Rα1表达明显增加(F=12.06,P＜0.05).结论 在REM睡眠剥夺和恢复过程中,GABA能系统存在自身调节机制,但无论是其再摄取抑制剂NO-711还是受体竞争剂SR-95531,均对认知功能下降产生不利影响,因此GABA能系统并不是治疗失眠的最理想靶点.Hcrt能神经元系统和GABA能系统之间存在相互抑制的作用,可以通过降低Hcrt神经元激活来改善睡眠的效果.并据此推断,Hcrt能系统可能是诱导睡眠和治疗失眠的潜在理想靶点.     

Comparison of the sleep pattern throughout a protocol of chronic sleep restriction induced by two methods of paradoxical sleep deprivation

The purpose of the present study was to evaluate the sleep homeostasis of rats submitted to a protocol of chronic sleep restriction by two methods and to evaluate the sleep characteristics during the recovery period. The sleep restriction protocol was accomplished by sleep depriving rats for 18 h everyday for 21 days, using the single platform method (SPM) or the modified multiple platform method (MMPM) of paradoxical sleep (PS) deprivation. Rats were allowed to sleep for 6 h (from 10:00 to 16:00; starting 3 h after lights on) in their individual home-cages, during which their sleep was recorded. At the end of the sleep restriction protocol, rats were recorded in their home-cages for 4 days, where they could sleep freely. Both methods used to induce chronic sleep restriction were effective, in sofar as they resulted in augmented sleep time during the 6h-sleep period, with very few bouts of wakening. Although comparison between the methods did not reveal differences, sleep restriction under MMPM produced a more consistent daily rebound, mainly of paradoxical sleep, with longer episodes. These results showed distinct sleep recovery patterns, suggesting a possible role of the waking experiences (i.e. immobilization stress, social interaction) acting on sleep consolidation.     

遗忘型轻度认知损害患者的前瞻性记忆障碍

目的 探讨遗忘型轻度认知损害(amnesia mild cognitive impairment,aMCI)患者前瞻性记忆(prospective memory,PM)改变的特征,初步了解基于事件的PM(event-based prospective memory,EBPM)和基于时间的PM(time-based prospective memory,TBPM)在aMCI患者中的损害情况.方法 建立PM的神经心理学测验方法,对30例aMCI患者以及年龄、受教育程度相匹配的30名健康老年人进行测试.结果 与健康对照组[EBPM:(2.33±0.66)分、TBPM:(4.90±1.03)分]相比,aMCI组的EBPM成绩[(0.90±1.09)分]和TBPM成绩[(4.23 ±1.14)分]差异均有统计学意义(t=-6.143,P<0.01;t=-2.383,P<0.05).结论 aMCI患者的记忆障碍不仅表现为回顾性记忆(retrospective memory,RM)损害,PM损害可能更为突出,且EBPM的损害程度大于TBPM和RM,提示EBPM的测查可能有利于aMCI的早期识别.     

脑梗死伴阻塞性睡眠呼吸暂停低通气综合征患者睡眠结构及认知功能分析

目的 探讨脑梗死伴阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者睡眠结构的特点及与认知功能的相关性.方法 选择2009年12月至2011年3月在天津医科大学总医院神经内科及呼吸睡眠监测室就诊的打鼾患者,行多导睡眠监测,筛选出60例患者,分为合并组(脑梗死合并OSAHS)20例,OSAHS组(单纯OSAHS)20例及对照组(无脑梗死及OSAHS)20例,均完善相关检查及进行认知功能的评分[ MMSE和蒙特利尔认知评估量表(MoCA)].结果 睡眠结构比较:合并组及OSAHS组与对照组比较,患者醒觉时间、非快速眼球运动(NREM)期、NREM 1+2期延长,NREM3+4期及快速眼球运动(REM)期缩短.合并组与OSAHS组比较,NREM期及NREM 1期延长,NREM 3+4及REM期缩短.认知功能与呼吸紊乱及低氧相关指数相关性分析:OSAHS组患者MMSE和MoCA评分与呼吸暂停低通气指数(AHI)、氧减指数(ODI)呈线性负相关(MMSE r=-0.450、-0.671,MoCA r=-0.486、-0.494,均P＜0.05),与夜间平均血氧及夜间最低血氧呈线性正相关(MMSE r=0.477、0.485,MoCA r=0.507、0.482,均P＜0.05).合并组患者MoCA评分与ODI、微觉醒指数呈线性负相关(r=-0.463、-0.480,均P＜0.05),MMSE评分与呼吸紊乱及低氧相关指数相关无统计学意义.认知功能与睡眠分期相关性分析:OSAHS组患者MMSE及MoCA评分均与NREM 3 +4期呈线性正相关(r=0.521、0.474,均P＜0.05),MMSE评分与NREM 1+2期呈线性负相关(r=-0.458,P＜0.05).合并组患者MoCA评分与REM期呈线性正相关(r=0.472,P＜0.05),MMSE评分与睡眠分期相关无统计学意义.结论 OSAHS患者睡眠结构紊乱,特点为觉醒时间与浅睡眠延长,深睡眠与REM期缩短,脑梗死伴OSAHS睡眠结构紊乱更严重,合并脑梗死使OSAHS浅睡眠1期延长更明显.OSAHS患者夜间血氧越低,呼吸紊乱指数越高,微觉醒次数越多,浅睡眠时间越长,深睡眠及REM期睡眠越短,认知功能受损越严重,但认知功能损害与低氧的相关性比睡眠结构紊乱的相关性明显.脑梗死伴OSAHS患者MoCA评分与缺氧程度及睡眠结构的一些指标相关性明显,MoCA在轻中度血管性认知功能障碍筛选中的敏感性高于MMSE.     

Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol

Numerous studies have evaluated the sleep homeostasis of rats after short- or long-periods of sleep deprivation, but none has assessed the effects of prolonged sleep restriction on the rat's sleep pattern. The purpose of the present study, therefore, was to evaluate the sleep homeostasis of rats under a protocol of chronic sleep restriction. Male Wistar rats were implanted with electrodes for EEG and EMG recordings. Using the single platform method, the animals were submitted to 18 h of sleep restriction, beginning at 16:00 h (lights on at 07:00 h), followed by a 6 h sleep window (from 10:00 h to 16:00 h) for 21 days. Immediately after this period, rats were allowed to sleep freely for 4 days (recovery period). The sleep–wake cycle was recorded throughout the entire experiment and the results showed that during the 6 h sleep window there was an increase on the percentage of sleep time, reflected by augmented time in high amplitude slow wave sleep and in paradoxical sleep, when compared to baseline sleep, whereas bouts of awakening longer than 1.5 min were greatly reduced, with the animals exhibiting a monophasic-type sleep pattern. During the deprivation period, paradoxical sleep was abolished. High amplitude slow wave sleep was also greatly affected by the protocol. Nonetheless, one day of recovery was sufficient to restore the normal sleep pattern. These findings indicate that this protocol was capable to induce many changes in the rat's sleep patterns, suggesting that during the 6 h sleep window there is a sleep adaptive homeostatic process.