The suprachiasmatic nucleus (SCN) is the primary circadian pacemaker in mammals. Individual SCN neurons can generate independent circadian oscillations of clock gene expression and neuronal firing, but SCN rhythmicity depends on sufficient membrane depolarization and intracellular calcium and cAMP. In the intact SCN, cellular oscillations are synchronized and reinforced by rhythmic synaptic input from other cells, resulting in a reproducible topographic pattern of distinct phases and amplitudes. The SCN network synchronizes its component cellular oscillators, reinforces their oscillations, responds to light input by altering their phase distribution, increases their robustness to genetic perturbations, and enhances their precision. Thus, even though individual SCN neurons can be cell-autonomous circadian oscillators, neuronal network properties are integral to normal function of the SCN. The SCN is a paired neuronal structure located in the anteroventral hypothalamus. It contains approximately 10,000 neurons in two anatomic subdivisions: a ventral "core" region and a dorsal "shell" region. The core projects densely to the shell, which projects sparsely back to the core. Neurons in the core and shell have distinct neurochemical content. The SCN generates pronounced circadian rhythms in frequency of spontaneous neuronal firing when physically isolated. The firing rhythm in SCN neurons is mediated partly by circadian regulation of membrane potassium channels. The SCN is composed of glial cells as well as neurons, and glia could potentially contribute to pacemaker function. Glial astrocytes exhibit circadian rhythms of clock gene expression. The SCN also generates circadian rhythms in output signals through circadian variation of neuronal firing and transmitter release at SCN axon terminals. SCN output signals are largely mediated by circadian variation of neuronal firing and transmitter release at SCN axon terminals, but some data also indicate a role for humoral output. The SCN synchronizes other oscillators throughout the brain and peripheral tissues. This is accomplished through diverse pathways, including autonomic neural connections and hormones. Rhythms in most tissues gradually damp out in the absence of the SCN. However, very sensitive reporters can still detect low amplitude rhythms in some tissues after many days in vitro, so local coupling mechanisms could still be present in some non-SCN tissues. SCN neurons are autonomous circadian oscillators, in the sense that they do not require rhythmic input from other cells to generate circadian rhythms of firing rate. The circadian period imposed by the SCN master pacemaker is determined at the level of a single cell. The SCN network reinforces cellular rhythmicity through rhythmic input from other cells in the network. The SCN network is more resistant to genetic perturbations than single SCN neurons. The period of the intact SCN pacemaker is more precise compared to the periods of independently oscillating SCN neurons. The SCN network is substantially more robust to certain genetic perturbations compared to SCN neurons that are oscillating independently in dispersedThe suprachiasmatic nucleus (SCN) is the primary circadian pacemaker in mammals. Individual SCN neurons can generate independent circadian oscillations of clock gene expression and neuronal firing, but SCN rhythmicity depends on sufficient membrane depolarization and intracellular calcium and cAMP. In the intact SCN, cellular oscillations are synchronized and reinforced by rhythmic synaptic input from other cells, resulting in a reproducible topographic pattern of distinct phases and amplitudes. The SCN network synchronizes its component cellular oscillators, reinforces their oscillations, responds to light input by altering their phase distribution, increases their robustness to genetic perturbations, and enhances their precision. Thus, even though individual SCN neurons can be cell-autonomous circadian oscillators, neuronal network properties are integral to normal function of the SCN. The SCN is a paired neuronal structure located in the anteroventral hypothalamus. It contains approximately 10,000 neurons in two anatomic subdivisions: a ventral "core" region and a dorsal "shell" region. The core projects densely to the shell, which projects sparsely back to the core. Neurons in the core and shell have distinct neurochemical content. The SCN generates pronounced circadian rhythms in frequency of spontaneous neuronal firing when physically isolated. The firing rhythm in SCN neurons is mediated partly by circadian regulation of membrane potassium channels. The SCN is composed of glial cells as well as neurons, and glia could potentially contribute to pacemaker function. Glial astrocytes exhibit circadian rhythms of clock gene expression. The SCN also generates circadian rhythms in output signals through circadian variation of neuronal firing and transmitter release at SCN axon terminals. SCN output signals are largely mediated by circadian variation of neuronal firing and transmitter release at SCN axon terminals, but some data also indicate a role for humoral output. The SCN synchronizes other oscillators throughout the brain and peripheral tissues. This is accomplished through diverse pathways, including autonomic neural connections and hormones. Rhythms in most tissues gradually damp out in the absence of the SCN. However, very sensitive reporters can still detect low amplitude rhythms in some tissues after many days in vitro, so local coupling mechanisms could still be present in some non-SCN tissues. SCN neurons are autonomous circadian oscillators, in the sense that they do not require rhythmic input from other cells to generate circadian rhythms of firing rate. The circadian period imposed by the SCN master pacemaker is determined at the level of a single cell. The SCN network reinforces cellular rhythmicity through rhythmic input from other cells in the network. The SCN network is more resistant to genetic perturbations than single SCN neurons. The period of the intact SCN pacemaker is more precise compared to the periods of independently oscillating SCN neurons. The SCN network is substantially more robust to certain genetic perturbations compared to SCN neurons that are oscillating independently in dispersed