Circadian rhythms in nocturnal and diurnal mammals are primarily synchronized to local time by the light-dark cycle. However, non-photic factors, such as behavioural arousal and metabolic cues, can also phase-shift the master clock in the suprachiasmatic nuclei (SCN) and/or reduce the synchronizing effects of light in nocturnal rodents. In diurnal rodents, the role of arousal or insufficient sleep in these functions is still poorly understood. In the present study, diurnal Sudanian grass rats, Arvicanthis ansorgei, were aroused at night by sleep deprivation (gentle handling) or caffeine treatment that both prevented sleep. Phase-shifts of locomotor activity were analyzed in grass rats transferred from a light-dark cycle to constant darkness and aroused in early night or late-night. Early, but not late night sleep deprivation induced a significant phase-shift. Caffeine on its own induced no phase-shifts. Both sleep deprivation and caffeine treatment potentiated light-induced phase-delays and phase-advances in response to a 30-min light pulse respectively. Sleep deprivation in early, but not late night potentiated light-induced c-FOS expression in the ventral SCN. Caffeine treatment in midnight triggered c-FOS expression in dorsal SCN. Both sleep deprivation and caffeine treatment potentiated light-induced c-FOS expression in calbindin-containing cells of the ventral SCN in early and late night. These findings indicate that, in contrast to nocturnal rodents, behavioural arousal induced either by sleep deprivation or caffeine during the sleeping period potentiates light resetting of the master circadian clock in diurnal rodents and activation of calbindin-containing suprachiasmatic cells may be involved in this effect.
|Journal||Journal of Neuroscience|
|Publication status||Published - Apr 2017|
- Journal Article