摘要
目的 探讨钙钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)在8 Br cAMP诱发的脊髓背角长时程增强(LTP)中的作用。方法 采用SD 大鼠, 常规细胞外记录技术记录脊髓背角腰膨大部位浅层C 纤维诱发电位。结果 ①8 Br cAMP(1 mmol/L)诱发的脊髓背角LTP咬合(occlude)强直刺激诱导的LTP;②CaMKⅡ选择性抑制剂KN 93 (100μmol/L)或AIP(200μmol/L)阻断8 Br cAMP诱导的脊髓背角LTP;③蛋白质合成抑制剂茴香霉素(200μmol/L)抑制8 Br cAMP诱发的脊髓LTP。结论 CaMKⅡ参与8 Br cAMP诱导的脊髓背角C 纤维诱发的LTP;8 Br cAMP诱导的LTP与强直电刺激诱导的LTP在机制上至少存在部分相同的步骤或途径。
Objective To explore the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMKII) on the induction of spinal long-term potentiation (LTP) induced by 8-Br-cAMP. Methods The C-fiber-evoked field potentials were recorded at the superficial layers of spinal dorsal horn at the lumbar enlargement. Results ① 8-Br-cAMP (1 mmol/L)-induced LTP of C-fiber evoked field potentials occluded the tetanus-induced LTP. ② Specific inhibitors of CaMKII, either KN-93(100 μmol/L) or AIP (200 μmol/L), completely blocked the induction of spinal LTP induced by 8-Br-cAMP. ③ The synaptic potentiation induced by 8-Br-cAMP was blocked in the presence of anisomycin(200μmol/L), an inhibitor of protein synthesis. Conclusion Activation of CaMKⅡ may be crucial for the induction of LTP of C-fiber-evoked field potentials in spinal dorsal horn induced by 8-Br-cAMP. It shares at least one or two steps in mechanisms of the 8-Br-cAMP-induced LTP and LTP produced by tetanic stimulation.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2005年第2期101-104,共4页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
国家自然科学基金资助项目(No.30200076
No.30070256)
