Validation of total sleep deprivation model in mice

• Published in: Sleep medicine 2013-12, Vol.14, p.e107-e107
• Main Authors: Dispersyn, G, Sauvet, F, Drogou, C, Ciret, S, Gallopin, T, Chennaoui, M
• Format: Article
• Language: English
• Subjects: Neurology; Sleep Medicine
• ISSN: 1389-9457; 1878-5506
• DOI: 10.1016/j.sleep.2013.11.233

Introduction Several models of sleep deprivation for rodents have been developed over years. One of the most relevant models is the activity wheel developed by Christie et al. for rats, presenting the advantages to induce few stress and physical activity. Even if this model is validated in rats, no data are available about its pertinence in mice. The aim of our study was to validate this model to mice by assessing that: i. the model do not generate high level of stress (determined by corticosterone assay and weight follow-up); ii. mice are awake 95% of time during sleep deprivation (determined by EEG); iii. the model induces a sleep rebound after sleep deprivation (determined by EEG, temperature and locomotor activity). Materials and methods 24 h total sleep deprivation (TSD) was produced by a slow rotational movement of an activity wheel programmed on a schedule of 3s “ on ” and 12s “ off ” in 13 male C57BL/6 mice. After sessions of wheel habituations, mice were exposed to a 24 h TSD (11 a.m.–11 a.m.). A first group of 8 mice were implanted with telemetry transmitter (TA10ETA-F20, DSI, USA) recording continuously EEG, locomotor activity and temperature before, during, and after 24 h TSD. At the end of 24 h TSD, mice of group 1 were recorded during 72 h to determine the sleep rebound and a second group of 5 mice were sacrificed to collect blood samples for corticosterone assay. A third group of 5 mice were not sleep deprived and were used as control, and sacrificed at the same time (11 a.m.). Results Corticosterone levels and weight curve were not different between control and sleep deprived mice. EEG recording during 24 h TSD shows that mice were awakened 97% of time. EEG recording after 24 h TSD show a significant sleep rebound by increasing quantity, non-REM sleep and delta power (0.5–4 Hz) during non-REM sleep, with no effect on REM sleep during the 24 h following TSD. Temperature and locomotor activity recording show a desynchronization of the two rhythms after 24 h TSD by modifying values of acrophase and amplitude. Conclusion Total sleep deprivation was effective by limiting mice sleep at 3% during 24 h, by inducing a sleep rebound during the 24 h following the end of privation (increase of non-REM sleep and delta power), and desynchronising locomotor activity and temperature rhythms. In conclusion, this model is as little stressful for mice as rats and can be used as a validated method for total sleep deprivation in rodents. Acknowledgement Directi