It has long been suspected that sensory signal transmission is inhibited in the mammalian brain during sleep. We hypothesized that Ca_v3.1 T-type Ca²⁺ channel currents inhibit thalamic sensory transmission to promote sleep. We found that T-type Ca²⁺ channel activation caused prolonged inhibition (>9 s) of action-potential firing in thalamic projection neurons of WT but not Ca_v3.1 knockout mice. Inhibition occurred with synaptic transmission blocked and required an increase of intracellular Ca²⁺. Furthermore, focal deletion of the gene encoding Ca_v3.1 from the rostral–midline thalamus by using Cre/loxP recombination led to frequent and prolonged arousal, which fragmented and reduced sleep. Interestingly, sleep was not disturbed when Ca_v3.1 was deleted from cortical pyramidal neurons. These findings support the hypothesis that thalamic T-type Ca²⁺ channels are required to block transmission of arousal signals through the thalamus and to stabilize sleep.