Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons

@article{Taylor2014InflammationEY,
  title={Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons},
  author={Bradley K. Taylor and Wen Fu and K. E. Kuphal and C-O. Stiller and Michelle K Winter and W. Chen and Gregory Corder and Janice H. Urban and Kenneth E. McCarson and Juan Carlos Marviz{\'o}n},
  journal={Neuroscience},
  year={2014},
  volume={256},
  pages={178-194}
}

Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn

It is concluded that Y1R-expressing excitatory dorsal horn interneurons facilitate neuropathic pain hypersensitivity, and this neuronal population remains sensitive to intrathecal NPY after nerve injury.

[Effects of blockade of 5-HT2A receptors in inflammatory site on complete Freund's adjuvant-induced chronic hyperalgesia and neuropeptide Y expression in the spinal dorsal horn in rats].

The present study suggests that the peripheral 5-HT2A receptors can be a promising target for pharmaceutical therapy to treat chronic inflammatory pain without central nervous system side effects.

An NPY Y1 receptor antagonist unmasks latent sensitization and reveals the contribution of Protein Kinase A and EPAC to chronic inflammatory pain.

PKA and Epac are sufficient to maintain long-lasting latent sensitization of dorsal horn neurons that is kept in remission by the NPY-Y1 receptor system, and two novel molecular signaling pathways in the dorsal horn that drive latent sensitized in the setting of chronic inflammatory pain are identified.

NPY2R signaling gates spontaneous and mechanical, but not thermal, pain transmission

The results suggest that Y1R could be a therapeutic target that may be exploited for alleviating spontaneous pain without affecting acute pain transmission and highlight the pivotal role of endogenous Y2R in gating mechanical and spontaneous pain transmission.

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