Davies S N, Lester R A, Reymann K G, Collingridge G L
Department of Pharmacology, University of Bristol, School of Medical Sciences, UK.
Nature. 1989 Apr 6;338(6215):500-3. doi: 10.1038/338500a0.
Long-term potentiation (LTP) in the hippocampus is widely studied as the mechanisms involved in its induction and maintenance are believed to underlie fundamental properties of learning and memory in vertebrates. Most synapses that exhibit LTP use an excitatory amino-acid neurotransmitter that acts on two types of receptor, the N-methyl-D-aspartate (NMDA) and quisqualate receptors. The quisqualate receptor mediates the fast synaptic response evoked by low-frequency stimulation, whereas the NMDA receptor system is activated transiently by tetanic stimulation, leading to the induction of LTP. The events responsible for maintaining LTP once it is established are not known. We now demonstrate that the sensitivity of CA1 neurons in hippocampal slices to ionophoretically-applied quisqualate receptor ligands slowly increases following the induction of LTP. This provides direct evidence for a functional post-synaptic change and suggests that pre-synaptic mechanisms also contribute, but in a temporally distinct manner, to the maintenance of LTP.
海马体中的长时程增强（LTP）受到广泛研究，因为其诱导和维持所涉及的机制被认为是脊椎动物学习和记忆基本特性的基础。大多数表现出LTP的突触使用一种兴奋性氨基酸神经递质，该递质作用于两种类型的受体，即N-甲基-D-天冬氨酸（NMDA）受体和quisqualate受体。quisqualate受体介导低频刺激诱发的快速突触反应，而NMDA受体系统则通过强直刺激短暂激活，从而导致LTP的诱导。LTP一旦建立，负责维持它的事件尚不清楚。我们现在证明，海马切片中CA1神经元对离子导入应用的quisqualate受体配体的敏感性在LTP诱导后会缓慢增加。这为突触后功能变化提供了直接证据，并表明突触前机制也有贡献，但以时间上不同的方式参与LTP的维持。
