鞘内注射神经激肽-1受体激动剂增强大鼠远位触液神经元pCaMK-IIα的表达  

INCREASE OF pCaMK-IIα IN THE DISTAL CSF-CONTACTING NEURONS BY INTRATHECAL [Sar^9,Met(O_2)^(11)]-SUBSTANCE P IN RAT

作　　者：王曙[1] 袁燕平[1] 褚智幸[1] 张励才[1] 

机构地区：[1]徐州医学院江苏省麻醉学重点实验室,江苏徐州221002

出　　处：《中国疼痛医学杂志》2009年第5期292-296,共5页Chinese Journal of Pain Medicine

基　　金：国家自然科学基金资助(No.30570974);江苏省自然科学基金资助(No:BK2004028)

摘　　要：目的:观察大鼠远位触液神经元在鞘内注射[Sar9,Met(O2)11]-substanceP(Sar-SP)致伤害性刺激信息调控中的作用。方法:CB-HRP大鼠侧脑室注射示踪标记dCSF-CN,鞘内注射Sar-SP(6.5nmol)造模,采用鞘内注射CaMK-IIα拮抗剂KN-93(10μM/10μl),注射人工脑脊液(artificial cerebrospinal fluid,aCSF)10μl作对照测定大鼠痛阈变化。以CB-HRP/pCaMK-IIα免疫组织化学法标记、定位CaMK-IIα在dCSF-CN的分布及表达变化。结果:鞘内注射Sar-SP后热板法大鼠痛阈明显降低,CB-HRP/pCaMK-IIα阳性细胞计数明显增多(P<0.01vsaCSF组);预先鞘内注射CaMK-IIα拮抗剂KN-93可部分抑制上述变化(P<0.01)。结论:鞘内注射Sar-SP可诱导dCSF-CN内CaMK-IIα的磷酸化并能被KN-93部分抑制,提示大鼠dCSF-CN可能通过CaMK-IIα参与伤害性刺激信息传递和信号调控。Objective： To investigate the involvement of the distal cerebrospinal fluid contacting neurons （dCSF-CNs） in modulation of nociceptive processing induced by[Sar^9 ,Met（O2）^11]-substance P （Sar-SP） in rat pain model. Methods： CaMK-Ⅱα/CB-HRP dual-labeling with immunohistochemical proce-dures to observe the distribution of CaMK-Ⅱα in dCSF-CNs and hot-plate was used to test the pain thresholds. Results： Intrathecal administration of Sar-SP showed decrease of pain threshold and the expression of phosphor-CaMK-Ⅱα in dCSF-CNs was increased at 10 min after Sar-SP injection, reached peak at 30 min, and remained a high level within 2h. Pretreatment of KN-93 attenuated the nociceptive behavior, decreased pain threshold and increased the expression of phosphor-CaMK-Ⅱα. Conclusions： Intrathecal administration of Sar-SP could increase the phosphorylation of CaMK-Ⅱα located in the dCSF-CNs and could be attenuated by pretreatment of KN-93, the results suggest that dCSF-CNs may be involved in the processing of nociception through CaMK-Ⅱα.

关 键 词：触液神经元 钙/钙调蛋白依赖的蛋白激酶 伤害性刺激 P物质 

分 类 号：R402[医药卫生—临床医学]