Nuclear calcium signaling in spinal neurons drives a genomic program required for persistent inflammatory pain.

ABSTRACT: Persistent pain induced by noxious stimuli is characterized by the transition from normosensitivity to hypersensitivity. Underlying mechanisms are not well understood, although gene expression is considered important. Here, we show that persistent nociceptive-like activity triggers calcium transients in neuronal nuclei within the superficial spinal dorsal horn, and that nuclear calcium is necessary for the development of long-term inflammatory hypersensitivity. Using a nucleus-specific calcium signal perturbation strategy in vivo complemented by gene profiling, bioinformatics, and functional analyses, we discovered a pain-associated, nuclear calcium-regulated gene program in spinal excitatory neurons. This includes C1q, a modulator of synaptic spine morphogenesis, which we found to contrib

SUBMITTER: Simonetti M 

PROVIDER: S-EPMC3593630 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature