中文摘要：

目的：观察大鼠远位触液神经元在鞘内注射[Sar^9，Met（O2）^11]-substance P（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，aCSr）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〈0.01 vs aCSF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。

英文摘要：

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.