Daily rhythmicity, including timing of wakefulness and hormone secretion, is mainly controlled by a master clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN clockwork involves various clock genes, with specific temporal patterns of expression that are similar in nocturnal and diurnal species (e.g. the clock gene Per1 in the SCN peaks at midday in both categories). Timing of sensitivity to light is roughly similar, during nighttime, in diurnal and nocturnal species. Molecular mechanisms of photic resetting are also comparable in both species categories. By contrast, in animals housed in constant light, exposure to darkness can reset the SCN clock, mostly during the resting period, i.e. at opposite circadian times between diurnal and nocturnal species. Nonphotic stimuli, such as scheduled voluntary exercise, food shortage, exogenous melatonin, or serotonergic receptor activation, are also capable of shifting the master clock and/or modulating photic synchronization. Comparison between day- and night-active species allows classifications of nonphotic cues in two, arousal-independent and arousal-dependent, families of factors. Arousal-independent factors, such as melatonin (always secreted during nighttime, independently of daily activity pattern) or γ-aminobutyric acid (GABA), have shifting effects at the same circadian times in both nocturnal and diurnal rodents. By contrast, arousal-dependent factors, such as serotonin (its cerebral levels follow activity pattern), induce phase shifts only during resting and have opposite modulating effects on photic resetting between diurnal and nocturnal species. Contrary to light and arousal-independent nonphotic cues, arousal-dependent nonphotic stimuli provide synchronizing feedback signals to the SCN clock in circadian antiphase between nocturnal and diurnal animals.