Activation of the cGMP/protein kinase G pathway by nitric oxide can decrease TRPV1 activity in cultured rat dorsal root ganglion neurons

Yunju Jin, Jun Kim, Jiyeon Kwak

Research output: Contribution to journalArticlepeer-review

Abstract

Recent studies have demonstrated that nitric oxide (NO) activates transient receptor potential vanilloid subtype 1 (TRPVl) via S-nitrosylation of the channel protein. NO also modulates various cellular functions via activation of the soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway and the direct modification of proteins. Thus, in the present study, we investigated whether NO could indirectly modulate the activity of TRPVl via a cGMP/PKG-dependent pathway in cultured rat dorsal root ganglion (DRG) neurons. NO donors, sodium nitroprusside (SNP) and S-nitro-N-acetylpenicillamine (SNAP), decreased capsaicin-evoked currents (Icap). NO scavengers, hemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO), prevented the inhibitory effect of SNP on Icap. Membrane-permeable cGMP analogs, 8-bromoguanosine 3′, 5′-cyclic monophosphate (8bromo-cGMP) and 8-(4chlorophenylthio)-guanosine 3′,5′-cyclic monophosphate (8-pCPT-cGMP), and the guanylyl cyclase stimulator YC-1 mimicked the effect of SNP on Icap. The PKG inhibitor KT5823 prevented the inhibition of Icap by SNP. These results suggest that NO can downregulate the function of TRPVl through activation of the cGMP/PKG pathway in peripheral sensory neurons.

Original languageEnglish (US)
Pages (from-to)211-217
Number of pages7
JournalKorean Journal of Physiology and Pharmacology
Volume16
Issue number3
DOIs
StatePublished - Jun 2012

Keywords

  • Dorsal root ganglion neuron
  • Nitric oxide
  • Protein kinase G
  • Rat
  • TRPVl

ASJC Scopus subject areas

  • Physiology
  • Pharmacology

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