Epac and nociceptor sensitization

Research output: Contribution to journalReview article

6 Scopus citations

Abstract

Primary sensory neurons are responsible for transmitting sensory information from the peripheral to the central nervous system. Their responses to incoming stimulation become greatly enhanced and prolonged following inflammation, giving rise to exaggerated nociceptive responses and chronic pain. The inflammatory mediator, prostaglandin E2 (PGE2), released from the inflamed tissue surrounding the terminals of sensory neurons contributes to the abnormal pain responses. PGE2 acts on G protein-coupled EP receptors to activate adenylyl cyclase, which catalyzes the conversion of adenosine triphosphate to cyclic adenosine 3′,5′-monophosphate (cAMP). Under normal conditions, cAMP activates primarily protein kinase A. After inflammation, cAMP also activates the exchange proteins activated by cAMP (Epacs) to produce exaggerated PGE2-mediated hyperalgesia. The role of cAMP-Epac signaling in the generation of hypersensitivity is the topic of this review.

Original languageEnglish (US)
JournalMolecular Pain
Volume13
DOIs
StatePublished - Jun 1 2017

Keywords

  • A-kinase anchor proteins
  • dorsal root ganglion
  • Epac
  • filamentous-actin
  • inflammation
  • nociception
  • protein kinase C
  • purinergic P2X3 receptor

ASJC Scopus subject areas

  • Molecular Medicine
  • Cellular and Molecular Neuroscience
  • Anesthesiology and Pain Medicine

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