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JoVE Journal Medicine

Medicine

Establishing a Device for Sleep Deprivation in Mice

Published: September 22, 2023 doi: 10.3791/65157
Automatic Translation
*1, *1, *2, *2, *2, 1,2
1Department of Cardiology, The First Affiliated Hospital of Bengbu Medical College, 2Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
* These authors contributed equally

Summary

The present protocol outlines a method for setting up a cost-effective rocker platform-based device used for inducing sleep deprivation in mice. This device has proven to be effective in causing disruptions in electroencephalogram (EEG)-evidenced sleep patterns, as well as inducing metabolic and molecular changes associated with sleep deprivation.

Abstract

Circadian rhythm disruption refers to the desynchronization between the external environment or behavior and the endogenous molecular clock, which significantly impairs health. Sleep deprivation is one of the most common causes of circadian rhythm disruption. Various modalities (e.g., platforms on the water, gentle handling, sliding bar chambers, rotating drums, orbital shakers, etc.) have been reported for inducing sleep deprivation in mice to investigate its effects on health. The current study introduces an alternative method for sleep deprivation in mice. An automated rocker platform-based device was designed that is cost-effective and efficiently disrupts sleep in group-housed mice at adjustable time intervals. This device induces characteristic changes of sleep deprivation with minimal stress response. Consequently, this method may prove useful for investigators interested in studying the effects and underlying mechanisms of sleep deprivation on the pathogenesis of multiple diseases. Moreover, it offers a cost-effective solution, particularly when multiple sleep deprivation devices are required to run in parallel.

Introduction

Circadian rhythm disruption refers to the desynchronization between the external environment or behavior and the endogenous biological clock. One of the most common causes of circadian rhythm disruption is sleep deprivation1. Sleep deprivation not only negatively affects human health but also significantly increases the risk of many diseases, including cancer2 and cardiovascular diseases3. However, the mechanisms underlying the detrimental effects of sleep deprivation remain largely unknown, and establishing sleep deprivation models is essential to enhance our understanding in this regard.

Various methods for sleep deprivation in mice have been reported, such as the use of water platforms4, gentle handling5, sliding bar chambers6, rotating drums7, and cage agitation protocols5,8,9. Sliding bar chambers automatically sweep bars across the bottom of the cage, forcing the mice to walk over them and stay awake. Cage agitation protocols involve placing cages on laboratory orbital shakers, resulting in efficient sleep disruption. While these methods are automatic and effective, they can be expensive when multiple devices are required to run in parallel, especially for specific study designs that involve a large number of sleep-deprived mice needed for circadian gene profiling. On the other hand, water platforms and gentle handling protocols are cheaper and simpler methods commonly used to induce sleep deprivation. However, the water platform does not allow automatic control of prespecified deprivation-rest cycles10,11, and gentle handling requires continuous vigilance from the researchers to disturb sleep. Additionally, other modalities, like rotating drums, can be confounded by social isolation or stress12.

Inspired by the orbital shaker-based method, we aim to introduce a protocol for establishing a rocker platform-based device for sleep deprivation in mice. This method is cheap, effective, minimally stressful, controllable, and automated. The current protocol allows us to create a rocker platform-based device at a cost approximately ten times cheaper than that of orbital shakers, based on our accessibility. This device effectively disrupted sleep in group-housed mice and induced characteristic changes of sleep deprivation with minimal stress response. It will be especially useful for researchers interested in investigating the effects and underlying mechanisms of sleep deprivation on the pathogenesis of multiple diseases, particularly when the study involves multiple-group sleep deprivation in parallel.

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Protocol

All animal experimental protocols in this study were approved by the Laboratory Animal Welfare Ethics Committee of Renji Hospital, School of Medicine, Shanghai Jiao Tong University. Male C57BL/6J mice, aged between 8 to 10 weeks, were used in the study. The animals were obtained from a commercial source (see Table of Materials). The major parts required for establishing the device are listed in Figure 1A.

1. Preparation of the sleep deprivation device

  1. Secure one end of a 50 cm slotted steel channel at the middle of a 40 cm slotted steel channel with screws (see Table of Materials) to make a T-shaped structure; repeat the process and make two such T-shaped structures (Figure 1B-a).
  2. Make the two T-shaped structures stand upwards parallelly 30 cm apart, and connect the bottoms of the two T-shaped structures with a 30 cm screw-compatible steel cylinder (see Table of Materials) using screws (Figure 1B-b).
  3. Place a steel rectangle platform (20 × 25 cm) (see Table of Materials) in between the two T-shaped structures (Figure 1B-c).
    NOTE: If ready-to-use steel rectangle platforms of the specified size are not available, one can make one by welding 2 mm thick flat steels.
  4. Secure each end of a 30 cm screw-compatible steel cylinder attached in the platform to two bearings fixed on each of the T-shaped structures at 10 cm down from the top (Figure 1B-d).
  5. Secure a motor mount (see Table of Materials) on one of the T-shaped structures at 25 cm down from the top using screws (Figure 1B-e).
    NOTE: Alternatively, construction adhesive can be used to secure the motor mount on the T-shaped structure instead of crews.
  6. Install a motor (see Table of Materials) on the motor mount with screws (Figure 1B-f).
  7. Secure a cooling fan (see Table of Materials) with self-locking bands on the T-shaped structure below the motor (Figure 1B-g).
  8. Fix the bearing end of a connecting rod to a platform corner facing the motor using screws (Figure 1B-h).
  9. Fix another end of the connecting rod to the shaft of the motor using screws (Figure 1B-i).
  10. Drill two 4 mm holes at each of the four corners of a plastic container or standard animal cage (see Table of Materials) using an electric drill, and drill two 4 mm holes and a lower 6 mm hole on the left side of the cage (Figure 1B-j).
  11. Secure the cage on the rectangle platform with self-locking bands through the corner holes (Figure 1B-k).
  12. Drill a 5 mm hole in the cap of a 50 mL centrifuge tube with an electric drill, and plug in the hole with a long nozzle equipped with a ball valve to prevent water leakage.
    NOTE: Hydrogel would be an alternative option for water supply if customizing water bottles is difficult.
  13. Secure the customized water bottle on the left side of the cage using self-locking bands through the two 4 mm holes, with the nozzle going through the 6 mm hole (Figure 1B-l).
  14. Connect the output electrical wires of the power brick adapter to the two terminals of the motor (Figure 1B-l).
    NOTE: There is no specific polarity requirement for connecting the wires to the motor terminals.
  15. Connect the input electrical wires of the power brick adapter to the time contactor (Figure 1B-m).

2. Induction of sleep deprivation

  1. Press the rightmost plus sign buttons on the left and right halves of the time contactor (see Table of Materials), respectively, until "M" appears on the mechanical counters on both sides (Figure 1C-a).
  2. Press the middle plus sign buttons on the left and right halves of the time contactor until "5M" appears on the mechanical counters on both sides (Figure 1C-b).
  3. Press the leftmost plus sign button on the left half of the time contactor until "15M" appears on the left mechanical counter (Figure 1C-c).
    ​NOTE: The time contactor will then be on for 15 min and off for 5 min in a cyclic mode.
  4. Put mice in the cage with water and food ad libitum.
  5. Supply the time contactor and the cooling fan with power.
    NOTE: The platform will now be rocking at 10 rpm.
  6. Weigh each mouse at Zeitgeber time 0 (ZT0) every day.
    ​NOTE: The light is on from 8 AM (ZT0) to 8 PM (ZT12).

3. Oral glucose tolerance test

  1. Measure the fasting glucose levels in fasted mice by sampling blood from tail veins.
  2. Inject glucose solution into each mouse (2 g/kg body weight) intraperitoneally using 1 mL syringes.
  3. Collect blood samples through the tail vein, and test the blood glucose at 15 min, 30 min, 60 min, and 120 min after glucose injection, respectively.
  4. Put the mice back into the cage with the food and water ad libitum after the test.

4. Harvesting the brain tissues

  1. Decapitate the mice after adequate anesthesia by exposing them to isoflurane (2%) for 3-5 min.
  2. Expose the skull and make a 1 cm vertical cut at the skull using surgical scissors.
  3. Remove the skull using mosquito hemostats (see Table of Materials) to expose the brain tissue.
  4. Gently move the whole brain out of the cranial cavity using curved tweezers.
    NOTE: Brain tissue should be removed according to local policies.
  5. Wash the brain tissue using cold phosphate-buffered saline (1x PBS, 4 °C).
  6. Snap freeze the intact brain tissue in liquid nitrogen and transfer the tissue to -80 °C for long-term storage .
    ​NOTE: When stored at -80°C, the flash-frozen brain tissue is stable for at least 6 months.

5. Detection of gene expression by polymerase chain reaction (PCR)

  1. Thaw the brain tissues at 4 °C or on ice.
  2. Transfer the tissue to a 1.5 mL microcentrifuge tube, and extract the total RNA using the TRIzol-based method13.
  3. Measure the concentration of RNA using a spectrophotometer (see Table of Materials) after RNA extraction.
  4. Perform reverse transcription of the total RNA (1 µg) into complementary DNA (cDNA) using a commercial kit14.
  5. Measure gene expression levels by real-time reverse transcription polymerase chain reaction15.

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Representative Results

The established device for sleep deprivation in mice is shown in Figure 1D. At day 7 after sleep deprivation commencement, electroencephalogram (EEG) and electromyography (EMG) monitoring16 indicated that the device significantly reduced sleep duration and increased wakefulness duration in mice (Figure 2A-D). Meanwhile, the current protocol significantly increased adenosine build-up and mRNA levels of Homer1a in the brain (Figure 2E,F), which are markers of successful sleep deprivation17. Using an ELISA kit18, we observed that serum corticosterone levels were not significantly changed by the current sleep deprivation protocol (Figure 2G). Following sleep deprivation for 7 days, body and thymus weight significantly decreased (Figure 3A-D), consistent with previous reports19. Moreover, glucose tolerance was significantly impaired in mice after sleep deprivation (Figure 3E,F). To investigate the changes in clock gene expression, brain tissues were collected every 4 h throughout a day. We observed that the expression patterns of the clock genes in the brain were significantly changed after sleep deprivation (Figure 3G and Table 1), suggesting disruption of the molecular clock20.

Figure 1
Figure 1: Establishment of the rocker platform-based device. (A) Illustrations depicting the major parts required for assembling the rocker platform-based device. (B) Detailed steps demonstrating the assembly of the sleep deprivation device. (C) Images displaying parameter settings in the time contactor. (D) Photograph of the fully assembled shaking chamber. Please click here to view a larger version of this figure.

Figure 2
Figure 2: Evaluation of sleep disturbance and serum corticosterone levels in mice. (A) Schematic diagram illustrating EEG/EMG recording in mice during sleep deprivation. (B) Representative EEG/EMG recordings traced in mice. (C) Representative EEG/EMG waveforms in mice during wakefulness, NREM, and REM. (D) Percentage of wakefulness duration, NREM duration, and REM duration recorded in sleep-disrupted mice and control mice (n = 4 mice/group). *P < 0.05, ***P < 0.001. Statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; NREM, Non-rapid eye movement; REM, Rapid eye movement; SD, sleep deprivation group. (E) mRNA levels of Homer1a in brain tissues measured in sleep-disrupted mice and control mice (n=4 mice/group). *P < 0.05, Statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; Homer1a, Homer scaffolding protein 1a; SD, sleep deprivation group. (F) Adenosine content in brain tissue measured in sleep-disrupted mice and control mice (n=4 mice/group) using an ELISA kit. *P < 0.05, Statistical analysis was performed using unpaired t-test at each time point. Abbreviations: CTR, control group; SD, sleep deprivation group. (G) Serum corticosterone concentration measured in sleep-disrupted mice and control mice (n = 4 mice per time point/group). Statistical analysis was performed using two-way analysis of variance. Abbreviations: CTR, control group; SD, sleep deprivation group. Please click here to view a larger version of this figure.

Figure 3
Figure 3: Pathophysiological changes after sleep deprivation in mice. (A) Representative images showing the sizes of mice in the indicated groups. Abbreviations: CTR, control group; SD, sleep deprivation group. (B) Changes in body weight after the initiation of sleep deprivation in the indicated groups (n = 24 mice per group). **P < 0.001, statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; SD, sleep deprivation group. (C) Representative images showing the sizes of the thymus in the indicated groups. Abbreviations: CTR, control group; SD, sleep deprivation group. (D) Comparison of the ratios of thymus weight to body weight between the two groups (n = 24 mice per group). **P < 0.001, statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; SD, sleep deprivation group. (E) Intraperitoneal glucose tolerance test results in the indicated groups (n = 5 per group). *P < 0.01; **P < 0.001, statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; SD, sleep deprivation group. (F) Comparison of the area under the curve (AUC) of the intraperitoneal glucose tolerance test between the sleep deprivation group and the control group (n = 5 per group). **P < 0.001, statistical analysis was performed using an unpaired t-test. Abbreviations: CTR, control group; SD, sleep deprivation group. (G) Circadian expression patterns of the clock genes (Bmal1, Dbp, Cry1, Cry2, Nr1d1, Nr1d2, Per1, and Per2) in brain tissues were measured in the sleep deprivation group and control group (n = 4 mice per time point/group). Data were compared using non-linear cosinor regression, and the expression curves of the clock genes were fitted using the R package CircaCompare. P-values are provided as indicated. Abbreviations: A, amplitude; Bmal1, brain and muscle Arnt-like 1; Cry1, cryptochrome circadian regulator 1; Cry2, cryptochrome circadian regulator 2; CTR, control group; Dbp, D-site binding protein; M, mesor; Nr1d1, nuclear receptor subfamily 1 group D member 1; Nr1d2, nuclear receptor subfamily 1 group D member 2; P, phase; Per1, period circadian regulator 1; Per2, period circadian regulator 2; SD, sleep deprivation group. Please click here to view a larger version of this figure.

Clock genes Bmal Dbp Cry1 Cry2 Nr1d1 Nr1d2 Per1 Per2
Rhythmicity Control P < 0.05 P < 0.01 P < 0.001 P < 0.05 P < 0.001 P < 0.01 P < 0.001 P < 0.001
Sleep deprivation P < 0.05 P < 0.001 P < 0.001 P < 0.001 P < 0.001 P < 0.001 P < 0.001 P < 0.001
Acrophase (Zeitgeber time) Control 22 12 17 15 11 14 14 16
Sleep deprivation 10 24 4 3 22 0 1 1
Mesor estimate Control 0.933 2.242 1.136 1.171 1.799 1.41 1.289 1.033
Sleep deprivation 0.826 2.101 1.094 1.155 1.756 1.399 0.999 0.888
Amplitude estimate Control 0.099 0.746 0.305 0.131 0.494 0.314 0.294 0.341
Sleep deprivation 0.108 0.866 0.342 0.168 0.503 0.323 0.388 0.305

Table 1: The presence of the rhythmicity, mesor estimate, amplitude estimate, and the acrophase for the tested clock genes in each group.

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Discussion

Mouse models of sleep deprivation are essential for studying the effects of sleep disruption on various diseases, including cardiovascular disease21, psychiatric conditions22, and neurological disorders23. Among the existing sleep deprivation strategies in mice, physical approaches that involve repetitive short-term interruption of sleep are the most commonly used5,7,12. These physical approaches include the use of water platforms4, gentle handling5, sliding bar chambers6,24, rotating drums7, or orbital shakers8,9,25,26.

To induce sleep deprivation in mice effectively, ideal methods should awaken the mice with a non-stressful stimulus. The chosen device should also be automated and easily controllable to adjust the deprivation-rest cycles. Among the mentioned methods, the sliding bar chamber meets most of these requirements. However, it is expensive and may occasionally harm the mice. Another effective and minimally stressful method is the orbital shaker-based protocol7,8,9,25, where a cage is placed on a standard laboratory orbital shaker connected to a time controller, leading to repetitive sleep interruption. However, when specific study designs require multiple orbital shakers to run in parallel, the cost may become prohibitive for some research groups.

Inspired by the orbital shaker methods, the current study presents a detailed step-by-step protocol for establishing a rocker platform-based sleep deprivation equipment. Its cost is approximately one-tenth of laboratory orbital shakers, making it more accessible. The introduced device was validated to be effective in sleep deprivation in mice, as indicated by EEG/EMG monitoring data that showed significantly shortened sleep duration and increased sleep deprivation markers. Additionally, this rocker platform-based device did not significantly alter serum corticosterone levels in mice. Overall, we have introduced a new automated sleep deprivation device that is inexpensive, effective, minimally stressful, and controllable.

Despite its advantages, the current protocol has some limitations. Firstly, unlike ready-to-use commercially available devices, the sleep deprivation device introduced here requires assembly by the experimenters. However, detailed step-by-step protocols and illustrations have been provided to simplify the process. Secondly, not all the materials required for device establishment are commercially available, and some customization of materials may be necessary based on the specifications provided in this work. Thirdly, conventional water bottles used with the rocker platform may experience leakage, necessitating the use of customized water bottles to prevent this issue.

In conclusion, this study presents a cost-effective and efficient method for establishing an alternative device to induce sleep deprivation in group-housed mice. This protocol can aid researchers in investigating the effects and underlying mechanisms of sleep deprivation on a wide range of health conditions.

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Disclosures

The authors have nothing to disclose.

Acknowledgments

This work was supported by grants from the National Natural Science Foundation of China (82230014, 81930007, 82270342), the Shanghai Outstanding Academic Leaders Program (18XD1402400), the Science and Technology Commission of Shanghai Municipality (22QA1405400, 201409005200, 20YF1426100), Shanghai Pujiang Talent Program (2020PJD030), SHWSRS(2023-62), Shanghai Clinical Research Center for Aging and Medicine (19MC1910500), and Postgraduate Innovation Program of Bengbu Medical College (Byycxz21075).

Materials

Name Company Catalog Number Comments
1.5 mL microcentrifuge tube Axygen MCT-150-C-S
50 mL centrifuge tube NEST 602002
Adenosine ELISA kit Ruifan technology RF8885
Animal cage ZeYa tech MJ2
Blood glucose meter YuYue 580
C57BL/6J Mice JieSiJie Laboratory Animal N/A Age: 8-10 weeks
Connecting rod ShengXiang Tech N/A Length:  20 cm
Cooling fan LiMing EFB0805VH Supply voltage: 5 V; Power consumption: 1.2 W; Air flow: 26.92 cfm; Dimensions: 40 mm * 40 mm * 56 mm
Corticosterone ELISA kit Elabscience E-OSEL-M0001
EEG/EMG recording and analysis system Pinnacle Technology 8200-K1-iSE3
Isoflurane RWD 20071302
mosquito hemostats FST 13011-12 Surgical instrument
Motor and motor mount MingYang MY36GP-555 Supply voltage: 24 V dc; Shaft diameter: 8 mm; Maximum output torque: 100 Kgf.cm; Maximum output speed: 10 rpm
NanoDrop 2000c Thermo Scientific NanoDrop 2000c
Power brick adapter MingYang QiYe-0243 Input voltage: 110-220V ac; Output voltage: 24 V dc; Outputcurrent: 2 A; Cable length: 2 m
qPCR commercial kit Vazyme Q711-02
qPCR measurement equipment Roche 480
Rectangle platform attached with a screw-compatible steel cylinder Customized N/A Width: 20 cm; length: 25 cm; length of the cylinder: 30 cm, thickness: 2 mm
Reverse RNA to cDNA commercial kit Vazyme R323-01
Screw and nut Guwanji N/A Inner diameter: 6 mm, 12 mm
Screw-compatible steel cylinder Customized N/A Length: 300 mm
Slotted steel channels Customized N/A Length: 400 mm or 500 mm, thickness: 2 mm
Time contactor LiXiang DH48S-S Supply voltage: 110-220 V ac; Units measured: hours, minutes, seconds; Contact configuration: DPDT
TRIzol Vazyme R401-01

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References

  1. Yang, D. F., et al. Acute sleep deprivation exacerbates systemic inflammation and psychiatry disorders through gut microbiota dysbiosis and disruption of circadian rhythms. Microbiological Research. 268, 127292 (2023).
  2. Alanazi, M. T., Alanazi, N. T., Alfadeel, M. A., Bugis, B. A. Sleep deprivation and quality of life among uterine cancer survivors: systematic review. Supportive Care In Cancer : Official Journal of the Multinational Association of Supportive Care In Cancer. 30 (3), 2891-2900 (2022).
  3. Tobaldini, E., et al. Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases. Neuroscience and Biobehavioral Reviews. 74, 321-329 (2017).
  4. Arthaud, S., et al. Paradoxical (REM) sleep deprivation in mice using the small-platforms-over-water method: polysomnographic analyses and melanin-concentrating hormone and hypocretin/orexin neuronal activation before, during and after deprivation. Journal of Sleep Research. 24 (3), 309-319 (2015).
  5. Saré, R. M., et al. Chronic sleep restriction in developing male mice results in long lasting behavior impairments. Frontiers In Behavioral Neuroscience. 13, 90 (2019).
  6. Roman, V., Vander Borght, K., Leemburg, S. A., Vander Zee, E. A., Meerlo, P. Sleep restriction by forced activity reduces hippocampal cell proliferation. Brain Research. 1065 (1-2), 53-59 (2005).
  7. Zhao, H. Y., et al. Chronic sleep restriction induces cognitive deficits and cortical beta-amyloid deposition in mice via BACE1-antisense activation. CNS Neuroscience & Therapeutics. 23 (3), 233-240 (2017).
  8. Lord, J. S., et al. Early life sleep disruption potentiates lasting sex-specific changes in behavior in genetically vulnerable Shank3 heterozygous autism model mice. Molecular Autism. 13 (1), 35 (2022).
  9. Sinton, C. M., Kovakkattu, D., Friese, R. S. Validation of a novel method to interrupt sleep in the mouse. Journal of Neuroscience Methods. 184 (1), 71-78 (2009).
  10. Rotenberg, V. S. Sleep after immobilization stress and sleep deprivation: common features and theoretical integration. Critical Reviews in Neurobiology. 14 (3-4), 225-231 (2000).
  11. Kim, T. K., et al. Melatonin modulates adiponectin expression on murine colitis with sleep deprivation. World Journal of Gastroenterology. 22 (33), 7559 (2016).
  12. Barf, R. P., Scheurink, A. J. Sleep disturbances and glucose homeostasis. European Endocrinology. 7, 14-18 (2011).
  13. Rio, D. C., Ares, M., Hannon, G. J., Nilsen, T. W. Purification of RNA using TRIzol (TRI reagent). Cold Spring Harbor Protocols. 2010 (6), (2010).
  14. Libus, J., Štorchová, H. Quantification of cDNA generated by reverse transcription of total RNA provides a simple alternative tool for quantitative RT-PCR normalization. Biotechniques. 41 (2), 156-164 (2006).
  15. Nolan, T., Hands, R. E., Bustin, S. A. Quantification of mRNA using real-time RT-PCR. Nature Protocols. 1 (3), 1559-1582 (2006).
  16. Mang, G. M., et al. Evaluation of a piezoelectric system as an alternative to electroencephalogram/electromyogram recordings in mouse sleep studies. Sleep. 37 (8), 1383-1392 (2014).
  17. Maret, S., et al. Homer1a is a core brain molecular correlate of sleep loss. Proceedings of the National Academy of Sciences. 104 (50), 20090-20095 (2007).
  18. Li, K., et al. Olfactory deprivation hastens Alzheimer-like pathologies in a human tau-overexpressed mouse model via activation of cdk5. Molecular neurobiology. 53, 391-401 (2016).
  19. Sousa, M. E., et al. Invariant Natural Killer T cells resilience to paradoxical sleep deprivation-associated stress. Brain, Behavior, and Immunity. 90, 208-215 (2020).
  20. Zhao, Y., et al. Disruption of circadian rhythms by shift work exacerbates reperfusion injury in myocardial infarction. Journal of the American College of Cardiology. 79 (21), 2097-2115 (2022).
  21. Miller, M. A., Cappuccio, F. P. Inflammation, sleep, obesity and cardiovascular disease. Current Vascular Pharmacology. 5 (2), 93-102 (2007).
  22. Minkel, J., et al. Sleep deprivation potentiates HPA axis stress reactivity in healthy adults. Health Psychology. 33 (11), 1430 (2014).
  23. Bishir, M., et al. Sleep deprivation and neurological disorders. BioMed Research International. 2020, 5764017 (2020).
  24. Franken, P., Tobler, I., Borbély, A. A. Cortical temperature and EEG slow-wave activity in the rat: analysis of vigilance state related changes. Pflugers Archiv : European Journal of Physiology. 420 (5-6), 500-507 (1992).
  25. Li, Y., et al. Effects of chronic sleep fragmentation on wake-active neurons and the hypercapnic arousal response. Sleep. 37 (1), 51-64 (2014).
  26. Jones, C. E., et al. Early-life sleep disruption increases parvalbumin in primary somatosensory cortex and impairs social bonding in prairie voles. Science Advances. 5 (1), (2019).

Tags

Device For Sleep Deprivation In Mice Circadian Rhythm Disruption Sleep Deprivation Methods Modalities For Inducing Sleep Deprivation Automated Rocker Platform-based Device Adjustable Time Intervals Minimal Stress Response Effects Of Sleep Deprivation On Health Pathogenesis Of Multiple Diseases
Establishing a Device for Sleep Deprivation in Mice
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Cite this Article

Chen, J., Wei, J., Ying, X., Yang,… More

Chen, J., Wei, J., Ying, X., Yang, F., Zhao, Y., Pu, J. Establishing a Device for Sleep Deprivation in Mice. J. Vis. Exp. (199), e65157, doi:10.3791/65157 (2023).

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