Stimuli that make hamsters active, such as dark pulses or triazolam administration, also phase shift their circadian clocks, producing phase advances during the subjective day and phase delays during the subjective night. Activity or its correlate appears to be important in producing the shifts because preventing locomotion blocks the phase shifts associated with these stimuli. The physiological basis of clock resetting induced by activity is not fully understood. The serotonergic (5-HT) projection from the raphe to the suprachiasmatic nucleus (SCN) is a possible route by which nonphotic information could reach the pacemaker. Administration of 8-HYDROXY-2-(DI-N-PROPYLAMINO) TETRALIN HYDROBROMIDE (8-OH-DPAT), a 5-HT1A and 5-HT7 receptor agonist, at circadian time (CT) 8 produces phase advances in the circadian rhythms of hamsters. Before concluding that 5-HT mediates the effect of activity on the pacemaker, it must be shown that 5-HT agonist do not produce shifts simply because they make animals more active. Therefore, we investigated the contribution of activity to 8-OH-DPAT-produced shifts. Preventing hamsters from moving around after administering 8-OH-DPAT did not abolish phase shifts. Moreover, higher doses of 8-OH-DPAT diminished activity on the day of injection but did not affect the amplitude of phase shifts. Suprisingly, quipazine (a non specific 5-HT agonist), when injected in the middle of subjective day did not phase shift the activity rhythm of hamsters, as it has been reported to do in rats.