The suprachiasmatic nucleus (SCN) is the primary circadian pacemaker in mammals, responsible for generating and maintaining circadian rhythms. While individual SCN neurons can function as autonomous circadian oscillators, their synchronized activity is crucial for the SCN's normal function. The SCN network synchronizes cellular oscillators, reinforces their oscillations, responds to light input, increases robustness to genetic perturbations, and enhances precision. This synchronization is achieved through rhythmic synaptic input from other cells, resulting in a reproducible topographic pattern of distinct phases and amplitudes. The SCN's circadian rhythm is regulated by a core transcriptional feedback loop involving clock genes such as Per and Cry, and additional negative feedback loops involving REV-ERBα and other regulatory mechanisms. Intracellular circadian timekeeping is a complex genetic network involving interconnected negative feedback loops that regulate transcription of core clock genes and output genes. Membrane depolarization, intracellular calcium, and cAMP are also important regulators of the mammalian transcriptional clock, with neuronal firing rhythms in SCN slices being calcium-dependent. The SCN is composed of neurons and glial cells, with glial astrocytes exhibiting circadian rhythms of clock gene expression. Glial signaling can affect neuronal function in other brain areas, and disruptions in glial metabolism can disrupt neuronal firing rhythms in SCN slices. The SCN receives photic input from the retina, allowing it to synchronize to the day/night cycle, and generates a pronounced circadian rhythm of neuronal firing frequency, enabling it to synchronize other cells throughout the body. 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 through diverse pathways, including autonomic neural connections and hormones. Rhythms in most tissues gradually damp out in the absence of the SCN, but some non-SCN tissues can oscillate persistently without the SCN. SCN neurons can generate independent circadian oscillations, but they are designed to function as part of a network, relying on input from other cells to generate rhythms. The SCN's network properties are integral to its normal function, with coupling mechanisms allowing it to remain synchronized even in constant darkness. The SCN's circadian period is determined at the level of a single cell, and its network reinforces cellular rhythmicity, increases robustness to genetic perturbations, and enhances precision. The SCN network is more resistant to genetic perturbations than single SCN neurons, with the coupled network providing redundancy and increased robustness to noise and variance of single cell periods. The period of the intact SCN pacemaker is more precise compared to the periods of independently oscillating SCN neurons, with the SCN network determining a compromise period through interactions between neurons of different periods. The SCN's network properties, including coupling and synchronization, are essential for its function as a master circThe suprachiasmatic nucleus (SCN) is the primary circadian pacemaker in mammals, responsible for generating and maintaining circadian rhythms. While individual SCN neurons can function as autonomous circadian oscillators, their synchronized activity is crucial for the SCN's normal function. The SCN network synchronizes cellular oscillators, reinforces their oscillations, responds to light input, increases robustness to genetic perturbations, and enhances precision. This synchronization is achieved through rhythmic synaptic input from other cells, resulting in a reproducible topographic pattern of distinct phases and amplitudes. The SCN's circadian rhythm is regulated by a core transcriptional feedback loop involving clock genes such as Per and Cry, and additional negative feedback loops involving REV-ERBα and other regulatory mechanisms. Intracellular circadian timekeeping is a complex genetic network involving interconnected negative feedback loops that regulate transcription of core clock genes and output genes. Membrane depolarization, intracellular calcium, and cAMP are also important regulators of the mammalian transcriptional clock, with neuronal firing rhythms in SCN slices being calcium-dependent. The SCN is composed of neurons and glial cells, with glial astrocytes exhibiting circadian rhythms of clock gene expression. Glial signaling can affect neuronal function in other brain areas, and disruptions in glial metabolism can disrupt neuronal firing rhythms in SCN slices. The SCN receives photic input from the retina, allowing it to synchronize to the day/night cycle, and generates a pronounced circadian rhythm of neuronal firing frequency, enabling it to synchronize other cells throughout the body. 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 through diverse pathways, including autonomic neural connections and hormones. Rhythms in most tissues gradually damp out in the absence of the SCN, but some non-SCN tissues can oscillate persistently without the SCN. SCN neurons can generate independent circadian oscillations, but they are designed to function as part of a network, relying on input from other cells to generate rhythms. The SCN's network properties are integral to its normal function, with coupling mechanisms allowing it to remain synchronized even in constant darkness. The SCN's circadian period is determined at the level of a single cell, and its network reinforces cellular rhythmicity, increases robustness to genetic perturbations, and enhances precision. The SCN network is more resistant to genetic perturbations than single SCN neurons, with the coupled network providing redundancy and increased robustness to noise and variance of single cell periods. The period of the intact SCN pacemaker is more precise compared to the periods of independently oscillating SCN neurons, with the SCN network determining a compromise period through interactions between neurons of different periods. The SCN's network properties, including coupling and synchronization, are essential for its function as a master circ