Research ArticleNeuroscience

LIMK-Dependent Actin Polymerization in Primary Sensory Neurons Promotes the Development of Inflammatory Heat Hyperalgesia in Rats

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Science Signaling  24 Jun 2014:
Vol. 7, Issue 331, pp. ra61
DOI: 10.1126/scisignal.2005353

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Tuning the Threshold for Pain

Pain tells when we are hurt or sick. Some conditions, like inflammation, can make us overly sensitive to pain. Like all cells, the neurons that sense pain have a cytoskeleton, which is made up of proteins, such as filament-forming actin, and which is constantly being reorganized. The kinase LIMK prevents the actin filaments in the cytoskeleton from being disassembled, and Li et al. discovered that reducing the activity or amount of LIMK in pain-sensing neurons made rats less sensitive to pain caused by heat in paws that were inflamed. Pain-sensing neurons are more active when the channel TRPV1 detects painful stimuli, such as the chemical capsaicin in hot peppers, and the authors found that LIMK activity made TRPV1 respond more strongly to capsaicin.