Cyclic AMP mediates the prostaglandin E2-induced potentiation of bradykinin excitation in rat sensory neurons

M. Cui, G. D. Nicol

Research output: Contribution to journalArticlepeer-review

97 Scopus citations


Prostaglandins enhance the sensitivity of sensory neurons to excitatory chemical agents such as bradykinin. The intracellular transduction cascades mediating this potentiation remain largely unknown. We have examined the role of cyclic AMP in the prostaglandin E2-induced potentiation of sensory neurons. Pretreatment with agents that elevate intracellular cyclic AMP levels enhances the number of action potentials elicited by bradykinin in a manner analogous to that of prostaglandin E2. The prostaglandin E2-induced potentiation of the number of bradykinin-elicited action potentials is blocked by either inhibition of adenylyl cyclase or protein kinase A. Therefore, our results suggest that prostaglandin E2 activates adenylyl cyclase to increase intracellular cyclic AMP, which in turn activates protein kinase A. Presumably activation of protein kinase A leads to increased levels of protein phosphorylation that then contribute to the enhancement of neuronal sensitivity to excitatory chemical agents.

Original languageEnglish (US)
Pages (from-to)459-466
Number of pages8
Issue number2
StatePublished - May 1995


  • 8-(4-chlorophenylthio)-adenosine-3′:5′-cyclic monophosphate:
  • 9-(tetrahydro-2-furyl)adenine
  • CPT-cyclic AMP
  • cyclic AMP-dependent protein kinase
  • dorsal root ganglion
  • DRG
  • EGTA
  • ethyleneglycol-bis(β-amino-ethyl ether)- N,N,N′,N′-tetra-acetate
  • N-(2-hydroxy-ethyl)piperazine- N′-(2-ethanesulfonic acid)
  • PGE
  • PKA
  • PKI
  • prostaglandin E
  • protein kinase inhibitor
  • THFA

ASJC Scopus subject areas

  • Neuroscience(all)

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