Experimental Approach
The involvement of Cav3.2 and T-type channels was investigated using genetic and pharmacological inhibition to assess mechanical allodynia/hyperalgesia and edema development in two murine inflammatory pain models. The location of Cav3.2 involved in pain-like symptoms was studied in mice with Cav3.2 knocked out in C-low threshold mechanoreceptors (C-LTMR) and the use of ABT-639, a peripherally restricted T-type channel inhibitor. The anti-edematous effect of Cav3.2 inhibition was investigated in chimeric mice with immune cells deleted for Cav3.2. Lymphocytes and macrophages from either green fluorescent protein-targeted Cav3.2 or KO mice were used to determine the expression of Cav3.2 protein and the functional status of the cells.