The Experiment Study Of ERK Inhabitor On The Analgesic Effect And Mechanisms In CFA-induced Rat Pain Model

objective To observe the changes of glutamate transporters expression in complete Freund's adjuvant (CFA) induced arthritic pain model. Methods 100μl CFA was injected into the plantar surface of the left hind paw of the rat to induce the persistent inflammation. Mechanical and thermal allodynia was measured for 10 days. Glutamate transporters expression in spinal cord and DRG was observed by immunohistochemistry. Results CFA injection greatly reduced the rat mechanical and thermal threshold, especially in the first 3 days. Gradually, mechanical and thermal threshold could regain to 70% of the basal level in day 10 after CFA injection. GLT-1 and EAAC1 could be found in normal rat spinal cord and DRG. Following inflammation, GLT-1 and EAAC1 expression increased in the first 3 days and decreased to the basal level in day 7 and 10. Conclusions CFA injection can greatly reduce the rat mechanical and thermal threshold. GLT-1 and EAAC1 expression in spinal cord and DRG first increased and gradually decreased to normal level. Glutamate transporters may involve in the plasticity of the CNS in this CFA induced pain model.objective The aim of the study was to observe the effect of ERK inhibitor PD98059 on glutamate transporters expression in adjuvant-induced arthritic rat spinal cord and dorsal root ganglion. Methods 24 rats were randomly divided into 4 groups: control group, purely inflammation group, PD1 group and PD10 group. In control group, 100μl sodium chloride was injected into the plantar surface of the hind paw of the rats, DMSO 10μl was given intrathecally twice daily.In purely inflammation group, 100μl CFA was injected into the plantar surface of the hind paw of the rats, DMSO 10μl was given intrathecally twice daily. For PD1 and PD10 group, after 100μl CFA was injected into the plantar surface of the hind paw of the rats ,PD98059 1μg or 10μg was given intrathecally twice daily. Thermal and mechanical threshold was measured for 3 days. On day 3 after inflammation, glutamate transporters expression in spinal cord and DRG was measured by RT-PCR. Results Mechanical and thermal threshold was greatly reduced after CFA was injected in rat hindpaw. PD 98059 could improve the Mechanical and thermal threshold, yet there is no difference between group PD1 and PD10. GLT-1 and EAAC1 expression in spinal cord and DRG of pure inflammation group was significant higher compared to that of the other three groups. Except the GLT-1 expression in DRG of group PD1 was higher than that of control group. GLT-1 and EAAC1 expression in spinal cord and DRG of PD1 and PD10 group had no significant difference compare to that of controlgroup. GLT-1 and EAAC1 expression in spinal cord and DRG of PD1 group had no difference compare to that of PD10 group. Conclusions PD98059 reduces the CFA-induced the mechanical allodynia and thermal hyperalgia. It also reduced the expression of GLT-1 and EAAC1 in rat spinal cord and DRG.objective The aim of the study was to observe the effect of ERK inhibitor PD98059 on NR1 expression in adjuvant-induced arthritic rat spinal cord and dorsal root ganglion. Methods lOOul CFA was injected into the plantar surface of the left hind paw of the rat to induce the persistent inflammation in 18 rats. NR1 receptor expression in spinal cord and DRG was observed by immunohistochemistry. Another 24 rats were randomly divided into 4 groups;control group, purely inflammation group, PDl group and PD10 group. In control group, lOOul sodium chloride was injected into the plantar surface of the left hind paw of the rats, DMSO 10ul was given intrathecally twice daily. In purely inflammation group, lOOul CFA was injected into the plantar surface of the hind paw of the rats, DMSO lOul was given intrathecally twice daily. For PDl and PD10 group, after 100p.l CFA was injected into the plantar surface of the hind paw of the rats, PD98059 ljxg or lOjxg was given intrathecally twice daily. On day 3 after inflammation, NR1 expression in spinal cord and DRG was measured by RT-PCR. Results 1. NR1 receptor could be found in normal rat spinal cord and DRG. Following inflammation, NR1 receptor expression increased in the first 3 days and decreased to the basal level in day 7 and 10. 2. NR1 expression in spinal cord and DRG of pure inflammation group was significant higher compared to that of the other three groups. Except the NR1 expression in DRG of group PDl was higher than that of control group. NR1 expressionin spinal cord and DRG of PD1 and PD10 group had no significant difference compare to that of control group. NRl expression in spinal cord and DRG of PD1 group had no difference compare to that of PD10 group. Conclusions The NRl expression in the spinal cord and DRG in CFA-induced inflammation rat shows a diphase changes: first the expression increased and then decreased. The mechanism of PD98059 reduces the CFA-induced the mechanical allodynia and thermal hyperalgia may through its influence on the NRl expression.