CaMKII在8-Br-cAMP誘發的脊髓背角LTP中的作用

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(1mmol/L)-induced LTP of C-fiber evoked field potentials occluded the tetanus-induced LTP. ② Specific inhibitors of CaMKⅡ, either KN-93(100μmol/L) or AIP(200μmol/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 produced by tetanic stimulation.