Lauri Sari E, Palmer Mary, Segerstrale Mikael, Vesikansa Aino, Taira Tomi, Collingridge Graham L
Neuroscience Center and Department of Biological and Environmental Sciences, University of Helsinki, 00014 Helsinki, Finland.
Neuropharmacology. 2007 Jan;52(1):1-11. doi: 10.1016/j.neuropharm.2006.06.017. Epub 2006 Aug 21.
The study of long-term potentiation (LTP) has for many years been the centre of a raging debate as to whether the process is expressed by presynaptic or postsynaptic mechanisms. Here we present evidence that two forms of synaptic plasticity at CA3-CA1 synapses in the hippocampus are expressed by presynaptic changes. One form is short-term potentiation (STP) and the other a neonatal form of early-LTP (E-LTP). We review recent experimental data that suggests that this latter form of LTP involves an increase in the probability of neurotransmitter release (Pr). We describe how this is caused by the rapid down-regulation of a high affinity kainate receptor, which otherwise responds to ambient levels of l-glutamate by depressing Pr.
多年来，关于长时程增强（LTP）过程是由突触前机制还是突触后机制表达，一直是激烈争论的焦点。在此，我们提供证据表明，海马体中CA3-CA1突触处的两种突触可塑性形式是由突触前变化表达的。一种形式是短时程增强（STP），另一种是早期长时程增强（E-LTP）的新生形式。我们回顾了最近的实验数据，这些数据表明后一种形式的LTP涉及神经递质释放概率（Pr）的增加。我们描述了这是如何由高亲和力海人藻酸受体的快速下调引起的，否则该受体通过降低Pr来响应环境水平的L-谷氨酸。
