Fat nerves keep pain at bay

Inflammatory pain is a debilitating condition and a severe health burden; physiologically, it is a complex phenomenon with multiple contributing mechanisms. A new study published in The EMBO Journal reports that tissue inflammation results in local depletion of cholesterol in nociceptive nerves, causing a loss of lipid raft localization of a sodium channel Na v 1.9 and, ultimately, resulting in potentiation of its activity. The discovered effect contributes to the inflammatory overexcitability of peripheral nociceptive nerve terminals resulting in inflammatory hyperalgesia. Topical application of cholesterol-containing gels was able to offset this inflammatory pain mechanism thereby opening a novel avenue for therapeutic intervention.