Modulation by nitric oxide (NO) of capsaicin-induced calcium uptake into rat dorsal root ganglion neurons

Biochem Mol Biol Int. 1999 Mar;47(3):435-42. doi: 10.1080/15216549900201463.

Abstract

The regulatory role of nitric oxide in capsaicin-induced 45Ca2+ accumulation in dorsal root ganglion neuronal cultures was investigated. Capsaicin-activated calcium entry was subject to complicated tuning by NO-releasing agents sodium nitroprusside, spermine/NO complex and NO synthase inhibitor NG-nitro-L-arginine methyl ester in concentration and stimulation protocol-dependent manner. In contrast, these agents failed to change depolarization-induced calcium influx. In experiments using dithiothreitol and 5,5-dithio-bis-2-nitrobenzoic acid this modulation was independent of the oxidizing action of NO. It is suggested that NO exerts a novel feedback modulatory effects on capsaicin-induced calcium entry into rat DRG neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Capsaicin / analogs & derivatives
  • Capsaicin / pharmacology*
  • Dithionitrobenzoic Acid / metabolism
  • Dithionitrobenzoic Acid / pharmacology
  • Dithiothreitol / metabolism
  • Ganglia, Spinal / drug effects*
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Neurons / drug effects
  • Nifedipine / pharmacology
  • Nitric Oxide / pharmacology*
  • Nitroprusside / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Spermine / pharmacology
  • Verapamil / pharmacology

Substances

  • Nitroprusside
  • Spermine
  • Nitric Oxide
  • Dithionitrobenzoic Acid
  • Verapamil
  • Nifedipine
  • capsazepine
  • Capsaicin
  • Calcium
  • Dithiothreitol
  • NG-Nitroarginine Methyl Ester