Calcium-regulated chloride channel (CaCC) anoctamin-1 has been recently identified in neurons. In neurons, which express the Na+–K+–2Cl− cotransporter, activation of CaCCs increases firing frequency, by reversion between the Cl− equilibrium potential and the membrane resting potential, leading to membrane depolarization by Cl− extrusion from the cell. Although there are no reports of CaCCs present in the suprachiasmatic nuclei (SCN), the fact that Na+–K+–2Cl− cotransporter is present in SCN neurons, where it has been shown to be involved in the excitatory effects of γ-aminobutyric acid, together with the increase of neuronal firing rate induced by release of intracellular Ca2+ after administration of 100 nM ryanodine, leads us to determine whether CaCCs are present in the SCN. Immunohistochemistry and western blots show the expression of the CaCCs anoctamin-1 protein. Quantitative PCR demonstrated the expression of anoctamin-1 mRNA in the SCN. These results clearly indicate the presence of CaCC in SCN of rats.