The sleep-wake cycle and motor activity, but not temperature, are disrupted over the light-dark cycle in mice genetically depleted of serotonin.
We examined the role that serotonin has in the modulation of sleep and wakefulness across a 12-h:12-h light-dark cycle and determined whether temperature and motor activity are directly responsible for potential disruptions to arousal state. Telemetry transmitters were implanted in 24 wild-type mice (Tph2(+/+)) and 24 mice with a null mutation for tryptophan hydroxylase 2 (Tph2(-/-)). After surgery, electroencephalography, core body temperature, and motor activity were recorded for 24 h. Temperature for a given arousal state (quiet and active wake, non-rapid eye movement, and paradoxical sleep) was similar in the Tph2(+/+) and Tph2(-/-) mice across the light-dark cycle. The percentage of time spent in active wakefulness, along with motor activity, was decreased in the Tph2(+/+) compared with the Tph2(-/-) mice at the start and end of the dark cycle. This difference persisted into the light cycle. In contrast, the time spent in a given arousal state was similar at the remaining time points. Despite this similarity, periods of non-rapid-eye-movement sleep and wakefulness were less consolidated in the Tph2(+/+) compared with the Tph2(-/-) mice throughout the light-dark cycle. We conclude that the depletion of serotonin does not disrupt the diurnal variation in the sleep-wake cycle, motor activity, and temperature. However, serotonin may suppress photic and nonphotic inputs that manifest at light-dark transitions and serve to shorten the ultraradian duration of wakefulness and non-rapid-eye-movement sleep. Finally, alterations in the sleep-wake cycle following depletion of serotonin are unrelated to disruptions in the modulation of temperature.
John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan; Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan;
Julia Z
JZ
Solarewicz
John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan; Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
Mariana
M
Angoa-Perez
John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan; Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
Donald M
DM
Kuhn
John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan; Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan; Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan; jmateika@med.wayne.edu.
Jason H
JH
Mateika
D056044:Actigraphy; D000818:Animals; D001833:Body Temperature Regulation; D001921:Brain / Q000378:metabolism*; D002940:Circadian Rhythm; D004569:Electroencephalography; D005838:Genotype; D008297:Male; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009043:Motor Activity; D010641:Phenotype; D017440:Photoperiod; D012701:Serotonin / Q000172:deficiency*; D012894:Sleep Stages; D013686:Telemetry; D013997:Time Factors; D014365:Tryptophan Hydroxylase / Q000172:deficiency / Q000235:genetics; D014851:Wakefulness
D012701:Serotonin; C487802:Tph2 protein, mouse; D014365:Tryptophan Hydroxylase
electroencephalography; electromyography; non-rapid-eye-movement sleep; paradoxical sleep; telemetry