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Persistent itch often accompanies allergic contact dermatitis (ACD), but the underlying mechanisms remain largely unexplored. We previously demonstrated that CXCL10/CXCR3 signaling activated a subpopulation of cutaneous primary sensory neurons and mediated itch response after contact hypersensitivity (CHS), a murine model of ACD, induced by squaric acid dibutylester. The purpose of this study was to determine the ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch. In whole cell recordings, CXCL10 triggered a current in dorsal root ganglion (DRG) neurons innervating the area of CHS. This current was modulated by intracellular Cl - and blocked by the general Cl - channel inhibitors. Moreover, increasing Ca 2+ buffering capacity reduced this current. In addition, blockade of Cl - channels significantly suppressed CXCL10-induced Ca 2+ response. In behavioral tests, injection of CXCL10 into CHS site exacerbated itch-related scratching behaviors. Moreover, the potentiating behavioral effects of CXCL10 were attenuated by either of two Cl - channel blockers. Thus we suggest that the Cl - channel acts as a downstream target mediating the excitatory and pruritic behavioral effects of CXCL10. Cl - channels may provide a promising therapeutic target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate. NEW &amp; NOTEWORTHY The ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch are largely unexplored. This study revealed that CXCL10 evoked an ionic current mainly carried by Cl - channels. We suggest that Cl - channels are likely key molecular candidates responsible for the CXCL10-evoked neuronal activation and itch-like behaviors in a murine model of allergic contact dermatitis induced by the antigen squaric acid dibutylester. Cl - channels may emerge as a promising drug target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate.

Cl− channel is required for CXCL10-induced neuronal activation and itch response in a murine model of allergic contact dermatitis

Cl⁻ channel is required for CXCL10-induced neuronal activation and itch response in a murine model of allergic contact dermatitis