PTPα基因敲除对小鼠海马CA1区突触可塑性的影响  

Effects of protein tyrosine phosphatase α knock out on Hippocampal CA1 synaptic plasticity

作　　者：陈聚涛[1] 

机构地区：[1]中国科学技术大学生命科学学院

出　　处：《中国科学技术大学学报》2006年第7期695-699,共5页JUSTC

摘　　要：通过PTPα基因敲除(knock out)小鼠来研究海马突触可塑性的变化,在海马schaffercollateral-CA1通路中采用场电位记录的方法研究发现,与Wild Type相比较,基因敲除小鼠的Long Term Potentiation(LTP)增强而Long Term Depression(LTD)受到抑制,去增强效应消失,θ频率诱导的LTP增强,但是其基本的突触传递性质并没有发生变化.To investigate the role of PTPa in synaptic plasticity, the fEPSP in hippocampal CA1 region was recorded by using the gene targeting deletion mice. Long Term Potentiation （LTP） was significantly enhanced while Long Term Depression （LTD） and depotentiation was diminished in PTPα-/- mice compared with Wild Type slices. Theta burst stimulation which can induce largest LTP amplitude in hippocampus also induced higher LTP amplitude in PTPα-/- mice than WT mice in hippocampal CA1 region. But PTPα-/-; shows normal basal synaptic transmission and short term synaptic plasticity. The results indicate that PTPa plays a crucial role in bidirectional synaptic plasticity of the hippocampus, identification of the up- and downstream molecular mechanism should provide more insight into the process of learning and memory.

关 键 词：PTPα海马 基因敲除 LTP LTD 去增强 

分 类 号：Q421[生物学—神经生物学]