Phosphatidylinositol 3-kinase activates ERK in primary sensory neurons and mediates inflammatory heat hyperalgesia through TRPV1 sensitization.

@article{Zhuang2004Phosphatidylinositol3A,
  title={Phosphatidylinositol 3-kinase activates ERK in primary sensory neurons and mediates inflammatory heat hyperalgesia through TRPV1 sensitization.},
  author={Zhi-Ye Zhuang and Haoxing Xu and David E. Clapham and Ru-Rong Ji},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2004},
  volume={24 38},
  pages={
          8300-9
        }
}
Although the PI3K (phosphatidylinositol 3-kinase) pathway typically regulates cell growth and survival, increasing evidence indicates the involvement of this pathway in neural plasticity. It is unknown whether the PI3K pathway can mediate pain hypersensitivity. Intradermal injection of capsaicin and NGF produce heat hyperalgesia by activating their respective TRPV1 (transient receptor potential vanilloid receptor-1) and TrkA receptors on nociceptor sensory nerve terminals. We examined the… CONTINUE READING

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