中文摘要：

长时程增强（long—term potentiation，LTP）被认为是与学习记忆密切相关的神经突触可塑性的生物学基础，多种信号通路参与了LTP的诱导与维持。丝裂原活化蛋白激酶（mitogen—activated protein kinases，MAPK）级联信号通路是介导细胞反应的重要信号系统，是细胞外信号从细胞表面传导到细胞核内部的重要传递途径，在细胞的增殖、分化和调亡过程中发挥重要作用。研究表明，MAPK的上游调节物质和下游作用分子在神经元中广泛存在，MAPK级联信号通路通过磷酸化神经元参与LTP诱导与维持的多种受体和酶，进而发挥对LTP的调节作用，影响神经突触可塑性。该文综述了细胞外信号调节激酶（extracellular signal—regulated kinase，ERK）、c—Jun氨基端激酶（c-Jun N—terminal kinase，JNK）和p383条MAPK通路对LTP的调节作用。

英文摘要：

Long-term potentiation （LTP） of synaptic activity in the hippocampal is the most widely researched model of synaptic plasticity, which is believed to underlie the brain function of learning and memory. Mitogen-activated protein kinases （MAPK） respond to a variety of cellular and extracellular stimuli, such as growth factors, cytokines, extracellular mitogen and stresses. MAPK are involved in complex processes such as in cell differentiation, proliferation and programmed cell death. It has been reported that the up-stream regulators and downstream substrats of MAPKs still widely exist in the mature neuron. MAPKs cascade induces phosphorylation of many functional protein including some receptors and kinases that is associated with induction and maintain of the LTP in the neuron, indicating that MAPKs do play a crucial role in the synaptic plasticity. Extracellular signal-regulated kinase （ERK）, c-Jun N-terminal kinase （JNK） and p38 activity and its relationship with LTP are reviewed.