Mainen Z F, Jia Z, Roder J, Malinow R
Cold Spring Harbor Laboratory, New York 11724, USA.
Nat Neurosci. 1998 Nov;1(7):579-86. doi: 10.1038/2812.
The mechanisms responsible for enhanced transmission during long-term potentiation (LTP) at CA1 hippocampal synapses remain elusive. Several popular models for LTP expression propose an increase in 'use' of existing synaptic elements, such as increased probability of transmitter release or increased opening of postsynaptic receptors. To test these models directly, we studied a GluR2 knockout mouse in which AMPA receptor transmission is rendered sensitive to a use-dependent block by polyamine compounds. This method can detect increases during manipulations affecting transmitter release or AMPA receptor channel open time and probability, but shows no such changes during LTP. Our results indicate that the recruitment of new AMPA receptors and/or an increase in the conductance of these receptors is responsible for the expression of CA1 LTP.
海马体CA1区突触在长时程增强（LTP）过程中增强传递的机制仍不清楚。几种流行的LTP表达模型提出，现有突触元件的“使用”增加，例如递质释放概率增加或突触后受体开放增加。为了直接测试这些模型，我们研究了一种GluR2基因敲除小鼠，其中AMPA受体传递对多胺化合物的使用依赖性阻断敏感。这种方法可以检测到在影响递质释放或AMPA受体通道开放时间和概率的操作过程中的增加，但在LTP过程中没有显示出这种变化。我们的结果表明，新的AMPA受体的募集和/或这些受体电导的增加是CA1区LTP表达的原因。
