|
KMID : 0811720010050000176
|
|
Korean Journal of Physiology & Pharmacology
2001 Volume.5 No. 0 p.176 ~ p.0
|
|
|
The Role of Protein Kinase in the Persistent Nociception in the Rat with CFA-Induced Chronic Inflammation
|
|
Shin Hong-Kee
Lee Seo-Eun
Kim Jin-Hyuk
Kim Jong-Suk
|
|
|
Abstract
|
|
|
There is considerable evidence that protein kinase (PK), especially PKC, is implicated in the development and maintenance of persistent painful state. In the present study, we studied the effect of protein kinase inhibitors on the persistent nociceptive responses induced by intraplantar injection of complete Freund s adjuvant (CFA) in the rat. In the behavioral test, mechanical hyperalgesia was determined using a set of von Frey hair. We observed the effects of intrathecally administered H-7 (PKC inhibitor) and H-9 (PKA and PKG inhibitor) on the CFA-induced mechanical hyperalgesia 10-15 days after CFA injection. In the electrophysio logical studies, changes in the responses of dorsal horn neurons to A- and C-fiber stimulation and iontophoretically applied NMDA were recorded in the lumbar enlargement of the rat spinal cord, which showed mechanical hyperalgesia after CFA injection, and the effects of iontophoretically applied protein kinase inhibitor (H-7) on the sensitized dorsal horn neurons were studied. Injection of CFA into plantar surface significantly increased the paw thickness and mechanical sensitivity ipsilateral to the inflammation. Intrathecal administration of H-7 induced the sustained attenuation of mechanical hyperalgesia whereas H-9 did not have any inhibitory effect. This inhibitory action of H-7 lasted more than 60 minutes. H-7 also had strong inhibitory action on the responses of dorsal horn neuron to NMDA, and C-fiber stimulation without any effect on the response to A-fiber stimulation. These experimental findings from the electrophysiological and behavioral studies suggest that in the dorsal horn, protein kinase contributes to the maintenance of persistent mechanical hyperalgesia produced by peripheral inflammation.
Source: Korean J Physiol Pharmacol.2001 Dec;5(Suppl II):S98-S99
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
  
|