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Keywords:

  • Chemical pain;
  • mechanical pain;
  • neuropathic pain;
  • spinal nerve ligation (SNL);
  • thermal pain;
  • tonic inflammatory pain

Although T-type Ca2+ channels are implicated in nociception, the function of specific subtypes has not been well defined. Here, we compared pain susceptibility in mice lacking CaV3.2 subtype of T-type Ca2+ channels (CaV3.2−/−) with wild-type littermates in various behavioral models of pain to explore the roles of CaV3.2 in the processing of noxious stimuli in vivo. In acute mechanical, thermal and chemical pain tests, CaV3.2−/− mice showed decreased pain responses compared to wild-type mice. CaV3.2−/− mice also displayed attenuated pain responses to tonic noxious stimuli such as intraperitoneal injections of irritant agents and intradermal injections of formalin. In spinal nerve ligation-induced neuropathic pain, however, behavioral responses of CaV3.2−/− mice were not different from those of wild-type mice. The present study reveals that the CaV3.2 subtype of T-type Ca2+ channels are important in the peripheral processing of noxious signals, regardless of modality, duration or affected tissue type.