Effect of intrathecal ganglioside GM-1 on chronic central pain following spinal cord injury in rats
10.3760/cma.j.issn.0254-1416.2014.02.016
- VernacularTitle:鞘内注射神经节苷酯GM-1对大鼠脊髓损伤后慢性中枢性痛的影响
- Author:
Yonggang XIE
;
Aizhi LI
;
Xiuliang JIANG
;
Jiahai MA
- Publication Type:Journal Article
- Keywords:
Gangliosides;
Spinal cord injuries;
Pain;
Injections,spinal
- From:
Chinese Journal of Anesthesiology
2014;34(2):183-185
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of intrathecal ganglioside GM-1 on chronic central pain (CCP) following spinal cord injury in rats.Methods Thirty-two adult male Sprague-Dawley rats,weighing 220-250 g,in which intrathecal catheters were successfully implanted,were randomly divided into 4 groups (n =8 each) using a random number table:control group (group C); group CCP; normal saline group (group N) and ganglioside GM-1 group (group GM).CCP was induced according to modified Allen method in CCP,N and GM groups.In group GM,ganglioside GM-1 20 mg/kg was injected intrathecally once a day,for 5 consecutive days,starting from 14th day after CCP,while the equal volume of nomal saline 10 μl was injected intrathecally in group N.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 4,8,16,24 and 48 h after the end of administration.The rats were then sacrificedat at 7 d after the end of adminmistration and L1 segment of the spinal cord was removed for determination of the expression of NMDA receptor 1 (NR1) by immuno-histochemistry.Results Compared with group C,MWT and TWL were significantly decreased,and NR1 expression was up-regulated in CCP and N groups (P ＜ 0.01),and no significant changes were found in MWT,TWL and NR1 expression in group GM (P ＞ 0.05).Compared with group CCP,no significant changes were found in MWT,TWL and NR1 expression in group N (P ＞ 0.05),and MWT and TWL were significantly increased,and NR1 expression was down-regulated in group GM (P ＜ 0.05).Conclusion Ganglioside GM-1 can alleviate CCP following spinal cord injury in rats and inhibition of expression of NR1 in the spinal cord may be involved in the mechanism.
