In mammals, the suprachiasmatic nuclei (SCNs) function as a circadian pacemaker that drives 24-h rhythms in physiology and behavior. The SCN is a multicellular clock in which the constituent oscillators show dynamics in their functional organization and phase coherence. Evidence has emerged that plasticity in phase synchrony among SCN neurons determines (i) the amplitude of the rhythm, (ii) the response to continuous light, (iii) the capacity to respond to seasonal changes, and (iv) the phase-resetting capacity. A decrease in circadian amplitude and phase-resetting capacity is characteristic during aging and can be a result of disease processes. Whether the decrease in amplitude is caused by a loss of synchronization or by a loss of single-cell rhythmicity remains to be determined and is important for the development of strategies to ameliorate circadian disorders.