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• W2089282622 abstract "S287 Introduction: Protein kinase C (PKC) is a regulatory enzyme that phosphorylates a [micro sign] receptor coupled G inhibitory protein which is believed to be involved in the development of opioid tolerance. [1] Site specific PKC inhibition with intrathecal GF109203X has been shown to reduce formalin induced nociception. [2] and intrathecal calphostin C blocks the development of acute tolerance to delta-opioid agonists. [3] The purpose of this study was to examine the effect of site specific inhibition or activation of PKC on the development of tolerance to daily intrathecal injections of morphine in the rat. Methods: Following IRB approval, 28 male Sprague-Dawley rats (250-275g) had intrathecal polyethylene catheters (0.28 mm ID, 0.61 mm OD) implanted. Following catheter implantation animals displaying neurologic impairment were eliminated from the study. The animals were then randomly assigned to receive intrathecal bolus injections (8[micro sign]L) of GF109203X 1[micro sign]g, calphostin C 100ng, phorbol 12,13-dibutyrate (PDBu) 250ng or vehicle (DMSO 10% in 0.9% saline). Thirty minutes following the injections all animals received a second intrathecal injection of morphine 30nmol (11.4[micro sign]g). Analgesia testing (tail flick method) was performed prior to the first and second injections and thirty minutes following the second (morphine) injection. Injections were repeated daily for seven days. On day 8 all groups received a single injection of morphine 30nmol (11.4[micro sign]g). Latencies to withdrawal to the thermal stimulus were converted to % maximum possible effect (MPE). Data were analyzed using analysis of variance for repeated measures. Post-hoc testing was done using Bonferroni corrected t-tests. Data are displayed as mean +/- SE. (Figure 1)Figure 1Results: Tail flick latencies following the first injections did not differ from baseline at any time during the study. Analgesic tolerance was evident on day 7 in all groups except the animals receiving GF109203X. This effect was still evident 24 hours following the last injection of the PKC modulator GF109203X, and resulted in greater analgesia in the animals that had received GF109203X. Discussion: Inhibition of PKC at the ATP dependent binding site of the catalytic domain by the specific inhibitor GF109203X prevented the development of tolerance in rats receiving daily morphine bolus injections. Similar results were not seen with the inhibitor calphostin C or the activator PDBu which effect the DAG binding site of the regulatory domain. These data suggest a binding site specificity for the activation of PKC in the development of morphine tolerance." @default.
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• W2089282622 date "1998-02-01" @default.
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• W2089282622 title "GFX109203X A SPECIFIC PROTEIN KINASE C INHIBITOR PREVENTS THE DEVELOPMENT OF MORPHINE TOLERANCE IN RATS" @default.
• W2089282622 doi "https://doi.org/10.1097/00000539-199802001-00285" @default.
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