β-Catenin, together with LEF1/TCF transcription factors, activates genes involved in the proliferation and differentiation of neuronal precursor cells. In mature neurons, β-catenin participates in dendritogenesis and synaptic function as a component of the cadherin cell adhesion complex. However, the transcriptional activity of β-catenin in these cells remains elusive. In the present study, we found that in the adult mouse brain, β-catenin and LEF1 accumulate in the nuclei of neurons specifically in the thalamus. The particular electrophysiological properties of thalamic neurons depend on T-type calcium channels. Cav3.1 is the predominant T-type channel subunit in the thalamus, and we hypothesized that theCacna1ggene encoding Cav3.1 is a target of the LEF1/β-catenin complex. We demonstrated that the expression ofCacna1gis high in the thalamus and is further increased in thalamic neurons treatedin vitrowith LiCl or WNT3A, activators of β-catenin. Luciferase reporter assays confirmed that theCacna1Gpromoter is activated by LEF1 and β-catenin, and footprinting analysis revealed four LEF1 binding sites in the proximal region of this promoter. Chromatin immunoprecipitation demonstrated that theCacna1gproximal promoter is occupied by β-cateninin vivoin the thalamus, but not in the hippocampus. Moreover, WNT3A stimulation enhanced T-type current in cultured thalamic neurons. Together, our data indicate that the LEF1/β-catenin complex regulates transcription ofCacna1gand uncover a novel function for β-catenin in mature neurons. We propose that β-catenin contributes to neuronal excitability not only by a local action at the synapse but also by activating gene expression in thalamic neurons.