Interleukin-1α links peripheral Ca_V2.2 channel activation to rapid adaptive increases in heat sensitivity in skin.

ABSTRACT: Neurons have the unique capacity to adapt output in response to changes in their environment. Within seconds, sensory nerve endings can become hypersensitive to stimuli in response to potentially damaging events. The underlying behavioral response is well studied, but several of the key signaling molecules that mediate sensory hypersensitivity remain unknown. We previously discovered that peripheral voltage-gated Ca_V2.2 channels in nerve endings in skin are essential for the rapid, transient increase in sensitivity to heat, but not to mechanical stimuli, that accompanies intradermal capsaicin. Here we report that the cytokine interleukin-1α (IL-1α), an alarmin, is necessary and sufficient to trigger rapid heat and mechanical hypersensitivity in skin. Of 20 cytokines screened, on

SUBMITTER: Salib AN 

PROVIDER: S-EPMC10996502 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature