Kullmann D M
Department of Clinical Neurology, Institute of Neurology, London, England.
Neuron. 1994 May;12(5):1111-20. doi: 10.1016/0896-6273(94)90318-2.
Quantal analysis has provided evidence for a presynaptic contribution to long-term potentiation in hippocampal CA1 cells. This however leaves unexplained the observation that long-term potentiation has little or no effect on the NMDA receptor-mediated component of the synaptic signal. Here, I report that, in baseline conditions, the coefficient of variation of the AMPA/kainate receptor-mediated signal (CVA/K) is consistently larger than that of the NMDA component (CVNMDA), a result which can be explained if AMPA/kainate receptors are absent or nonfunctional at a proportion of synapses. Long-term potentiation is associated with a reduction in CVA/K, but no change in either the average amplitude of the NMDA component or CVNMDA. This is consistent with the proposal that long-term potentiation induction uncovers clusters of latent AMPA/kainate receptors, with no change in transmitter release.
量子分析为海马体CA1细胞中突触前对长时程增强的作用提供了证据。然而,这并未解释长时程增强对突触信号中NMDA受体介导成分几乎没有影响这一现象。在此,我报告,在基线条件下,AMPA/海人藻酸受体介导信号的变异系数(CVA/K)始终大于NMDA成分的变异系数(CVNMDA),如果在一定比例的突触中AMPA/海人藻酸受体缺失或无功能,这一结果就能得到解释。长时程增强与CVA/K的降低相关,但NMDA成分的平均幅度或CVNMDA均无变化。这与长时程增强诱导揭示了潜在AMPA/海人藻酸受体簇且递质释放无变化的提议一致。