Abstract
The processing of itch signals is regulated by many different ion channels. Among those are T-type calcium channels which are important regulators that contribute to the firing behavior of pruriceptors, or itch sensing neurons. The human genome encodes three different T-type channels: Cav3.1, Cav3.2, Cav3.3. It has been shown recently that pharmacological blockade of T-type calcium channels inhibits acute itch and that immune cells can express Cav 3 channels with roles in effector function. Thus, we hypothesized that local administration of the novel small molecule T-Type calcium channel inhibitor, DX416, would decrease cutaneous itch both through reducing pruriceptors signals triggering itch and decreasing local inflammatory immune responses potentiating itch.
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