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

M. Cui, Grant Nicol

Research output: Contribution to journalArticle

97 Citations (Scopus)

Abstract

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
Pages (from-to)459-466
Number of pages8
JournalNeuroscience
Volume66
Issue number2
DOIs
StatePublished - 1995

Fingerprint

Bradykinin
Sensory Receptor Cells
Dinoprostone
Cyclic AMP
Cyclic AMP-Dependent Protein Kinases
Adenylyl Cyclases
Action Potentials
Prostaglandins
Phosphorylation
Proteins

Keywords

  • 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
  • HEPES
  • N-(2-hydroxy-ethyl)piperazine- N′-(2-ethanesulfonic acid)
  • PGE
  • PKA
  • PKI
  • prostaglandin E
  • protein kinase inhibitor
  • THFA

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Cyclic AMP mediates the prostaglandin E2-induced potentiation of bradykinin excitation in rat sensory neurons. / Cui, M.; Nicol, Grant.

In: Neuroscience, Vol. 66, No. 2, 1995, p. 459-466.

Research output: Contribution to journalArticle

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abstract = "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.",
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