Key Results
We showed the role of Cav3.2 channels in the development
of pain-like symptoms and edema in the two murine inflammatory pain
models. For the first time, we provide evidence of the involvement of
Cav3.2 channels located on C-LTMRs in inflammatory pain
at both peripheral and primary afferent terminals at the spinal level.
We showed that Cav3.2 channels located in T cells and
macrophages contribute to the inflammatory process.