Instituto Cajal, CSIC, Avenida Doctor Arce 37, 28002-Madrid, Spain.
Hippocampus. 2011 Apr;21(4):374-85. doi: 10.1002/hipo.20754.
Long-term potentiation (LTP) has received attention because of its proposed role in learning and memory. Despite substantial effort the pre- or postsynaptic expression site of LTP remains unsettled. It has been proposed that LTP is expressed postsynaptically through the functional conversion of "silent synapses." We had shown that Schaffer collateral (SC) silent and "functional synapses," which lack and express AMPA receptors, respectively exhibit distinct transmitter release properties. Therefore the functional conversion of silent synapses with LTP should be associated with presynaptic modifications. We now show that the pairing-induced LTP at SC synapses is mediated by combined pre- and postsynaptic modifications involving the postsynaptic emergence of an AMPA response coupled with an enhanced glutamate release. BDNF replicates the changes associated with this LTP by activating TrkBRs, suggesting that the neurotrophin is required for the coordinated changes on both sides of the synaptic cleft.
长时程增强(LTP)因其在学习和记忆中的作用而受到关注。尽管已经付出了大量努力,但 LTP 的突触前或突触后表达位点仍未确定。有人提出,LTP 是通过“沉默突触”的功能转换在突触后表达的。我们已经表明,Schaffer 侧支(SC)沉默和“功能突触”分别缺乏和表达 AMPA 受体,表现出不同的递质释放特性。因此,沉默突触与 LTP 的功能转换应该与突触前修饰有关。我们现在表明,SC 突触的配对诱导的 LTP 是由涉及 AMPA 反应的突触后出现的联合突触前和突触后修饰介导的,同时伴随着谷氨酸释放的增强。BDNF 通过激活 TrkB Rs 复制与这种 LTP 相关的变化,表明神经营养因子对于突触裂隙两侧的协调变化是必需的。