Activation of cGMP-dependent protein kinase Iα is required for N-methyl-D-aspartate- or nitric oxide-produced spinal thermal hyperalgesia

Yuan Xiang Tao, Roger A. Johns

Research output: Contribution to journalArticlepeer-review

Abstract

The effect of a selective cyclic guanocine 3',5'-monophosphate (cGMP)-dependent protein kinase Iα inhibitor, Rp-8-[(4-chlorophenyl)thio]-cGMPS triethylamine (Rp-8-p-CPT-CGMPS), on either N-methyl-D-aspartate (NMDA)- or N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino)ethanamine (NOC-12, a nitric oxide (NO) donor)-produced thermal hyperalgesia was examined in the rat. Intrathecal administration of NMDA (15 pg/10 μl) or NOC-12 (10, 20 and 30 μg/10 μl) produced a marked curtailment of the tail-flick latency. Maximal NMDA- or NOC-12-produced facilitation of the tail-flick reflex was significantly and dose-dependently blocked by intrathecal pretreatment with Rp-8-p-CPT-CGMPS (7.5, 15 and 30 μg/10 μl). Rp-8-p-CPT-CGMPS given alone did not markedly alter baseline tail-flick latency. These results suggest that the activation of cGMP-dependent protein kinase Iα is required for NMDA- or NO-produced facilitation of thermal hyperalgesia at the spinal cord level. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)141-145
Number of pages5
JournalEuropean Journal of Pharmacology
Volume392
Issue number3
DOIs
StatePublished - Mar 31 2000

Keywords

  • Hyperalgesia
  • N-methyl-D-aspartate (NMDA)
  • Nitric oxide (NO)
  • Nociception
  • Pain
  • Protein kinase
  • Spinal cord
  • cGMP-dependent

ASJC Scopus subject areas

  • Pharmacology

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