SignificanceUnderstanding the pathophysiological mechanism of central neuropathic pain has attracted much attention, especially because neuropathic pain is often unresponsive to existing medical treatments. In this study, we investigated the role of CaV3.1 T-type Ca2+channels in the development of trigeminal neuropathic pain (TNP) in mice. Our results show that, intriguingly, CaV3.1 knockout mice had attenuated TNP. Specifically, we demonstrate that increased low-frequency rhythmicity and widely spread noncolumnar activity were present in wild-type TNP mice but not in knockout TNP mice. Moreover, abnormally pronounced coupling between low-frequency and high-frequency rhythms in the thalamocortical network of wild-type mice was absent in CaV3.1 knockout mice. Our results clearly imply that the presence of CaV3.1 channels is a crucial element in the pathophysiology of TNP.