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.