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Objective Effect of (-)clausenamide on potentiating field excitatory postsynaptic potential (f-EPSP) in CA1 region of rats hippocampal slice and its related mechanism were investigated in the paper.Methods 8 × 8 multi-electrode array probe was used to measure f-EPSP.The phosphorylation and expression of CaMKⅡα, ERK1/2, CREB were detected by Western blot.Results (-)Clausenamide facilitated synaptic plasticity at dose-dependent manner.And (-)clausenamide also activated CaMKⅡα and ERK1/2.Pretreatment with KN93 (CaMKⅡα inhibitor, 10 μM) for 20 min before (-)clausenamide addition completely blocked the enhancement of synaptic transimisson induced by (-)clausenamide.PD98059 (MEK inhibitor, 30 μM) partially blocked the effect of (-)clausenamide.And KN93 and PD98059 attenuated the activation of CREB induced by (-)clausenamide.Thus, the results suggested that CaMKⅡα-ERK1/2-CREB involved in the process of (-)clausenamide facilitating synaptic transmission.U73122, an inhibitor of PLCγ, attenuated the slop of f-EPSP before or after the treating of (-)clausenamide.Nimodipine blocked partially the effect of (-)clausenamide by pre-incubation, but showing no difference with basic value when treated after the perfusion of (-)clausenamide.The data indicated that external calcium influx induced by (-)clausenamide was necessary for initiating synaptic transmission and calcium influx induced by (-)clausenamide may promote the release ofintracellular calcium responsible for synaptic enhancement.Conclusion (-)clausenamide promoted calcium influx to initiating synaptic transmission and triggering intracellular calcium release, and subsequently activated CaMKⅡα-ERK1/2-CREB signal pathway.