Low threshold Ca2+ currents mediated by T-type channels underlie burst spike activities of relay neurons in the thalamus. We have previously reported that knock-out mice for T-type channels show an enhanced nociceptive response to visceral pain, accompanied by an increase in tonic spikes in the absence of burst spikes in thalamic relay neurons. These results raised a possibility that T-type channels are involved in thalamic sensory gating, blocking the relay of the pain signals to the cortex. We have tested this hypothesis by using several different sensory modalities: startle responses to auditory or tactile stimuli, and the response to chronic inflammatory pain. First, the mutant mice showed an enhanced startle response to auditory stimulations. The auditory brainstem recording (ABR) results indicated that the enhanced response was not due to increased input signals from the cochlear to the brainstem. Second, the mutant also displayed an enhanced startle response to tactile stimuli. Third, the mutant showed a selective increase in the late phase response to an intradermal injection of formalin into the hind paw, which known to be controlled by a supraspinal mechanism. Therefore, the mutant showed enhanced responses to sensory inputs of four different modalities, strongly supporting the idea that T-type channels are required in thalamic sensory gating. We suggest that the burst spikes induced by the low threshold Ca2+ currents are the key element in this thalamic function. Furthermore, the mutant mice showed mania-like behaviors, an increased alcohol preference, and resistance to alcohol-induced hypnotic effect. These behavioral consequences will be discussed with regard to the sensory gating failure of the mutant.