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Sleep-dependent cardiovascular control in mouse models of obesity and narcolepsy| old_uid | 10066 |
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| title | Sleep-dependent cardiovascular control in mouse models of obesity and narcolepsy |
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| start_date | 2011/06/15 |
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| schedule | 11h |
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| online | no |
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| location_info | Faculté de Médecine Lyon Est, esc. E - 8 a, 3è étage, salle de réunion |
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| details | Conférence CRNL - Equipe Juan-Sheng Lin |
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| summary | Central autonomic commands associated with wake-sleep cycles play a major role in generating cardiovascular variability at ultradian and circadian time scales. Values of blood pressure during sleep and the blood pressure difference between wakefulness and sleep carry prognostic information in patients and the general population. Mice are currently the species of choice to investigate functional cardiovascular and sleep genomics. Technical developments allow simultaneous long-term recordings of sleep (electroencephalographic and electromyographic electrodes), heart rate, and blood pressure (telemetric blood pressure transducer) in freely behaving mice. This technique was first applied on ob/ob mice, which are morbidly obese because of congenital leptin deficiency. Results demonstrated that in on/ob mice, hypertensive blood pressure derangements depend on the wake-sleep state, occurring in wakefulness and non-rapid-eye-movement sleep (NREMS) but not in rapid-eye-movement sleep (REMS), and are compensated during the dark (active) day period by an increase in the time spent asleep. Ob/ob mice also show sleep-dependent derangements in the control of heart rhythm, with a decrease in cardiac vagal modulation that is most prominent during NREMS and REMS. More recently, cardiovascular phenotyping during sleep was performed on hypocretin-deficient mouse models of narcolepsy (hypocretin knock-out mice lacking hypocretin peptides and hypocretin-ataxin3 transgenic mice lacking hypocretin neurons). Results showed that in both mouse models, hypocretin deficiency blunts the physiological decrease in blood pressure on passing from wakefulness to sleep, this effect being most prominent and robust to changes in genetic background during REMS. In conclusion, these studies demonstrated that cardiovascular derangements occur in mouse models of obesity and narcolepsy and are substantially modulated by the behavioral wake-sleep phenotype. |
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| responsibles | Béranger, Rossetti |
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