神经元的突触可塑性与学习和记忆

大量研究表明,神经元的突触可塑性包括功能可塑性和结构可塑性,与学习和记忆密切相关.最近,在经过训练的动物海马区,记录到了学习诱导的长时程增强(long term potentiation,LTP),如果用激酶抑制剂阻断晚期LTP,就会使大鼠丧失训练形成的记忆.这些结果指出,LTP可能是形成记忆的分子基础.因此,进一步研究哺乳动物脑内突触可塑性的分子机制,对揭示学习和记忆的神经基础有重要意义.此外,在精神迟滞性疾病和神经退行性疾病患者脑内记录到异常的LTP,并发现神经元的树突棘数量减少,形态上产生畸变或萎缩,同时发现,产生突变的基因大多编码调节突触可塑性的信号通路蛋白,故突触可塑性研究也将促进精神和神经疾病的预防和治疗.综述了突触可塑性研究的最新进展,并展望了其发展前景.

Neuronal Synaptic Plasticity, Learning and Memory

Extensive studies have indicated that synaptic plasticity of neurons, including functional and structural plasticity, is intimately related to learning and memory. Recently, a long-term potentiation (LTP) induced by learning was successfully recorded in hippocampal neurons of the trained rats, which lost their retention memory if the late LTP was blocked by a kinase inhibitor. These results show that LTP may be a molecular mechanism underlying memory. Therefore, further studies on synaptic plasticity in the mammalian brain are of significance to revealing molecular mechanisms underlying learning and memory. Furthermore, abnormal morphology, shrinkage and reduced density of dendritic spines and defects in LTP were observed in brains of the patients suffering from mental retardation and neurodegenerative diseases; many mutant genes found from these patients encode component proteins of signal transduction for neuronal plasticity. These studies on synaptic plasticity would certainly promote making the effective prevention and treatment procedures for mental and neurodegenerative diseases. Advances in synaptic plasticity studies and looks into the future of this research field are reviewed.