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Abstract
The effect of a selective cyclic guanocine 3',5'-monophosphate (cGMP)-dependent protein
kinase Ialpha 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 microl) or NOC-12 (10, 20 and
30 microg/10 microl) 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 microg/10 microl). 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 Ialpha is required for NMDA- or NO-produced facilitation of thermal hyperalgesia
at the spinal cord level.