Voronin L L, Volgushev M, Chistiakova M, Kuhnt U, Singer W
Brain Research Institute, Russian Academy of Medical Sciences, Moscow, Russia.
Neuroscience. 1996 Sep;74(2):323-30. doi: 10.1016/0306-4522(96)00207-2.
Changes in the latency of small excitatory postsynaptic potentials were observed in association with induction of long-term modifications of synaptic transmission in slices of rat neocortex and guinea-pig hippocampus. After potentiation response latency decreased in 3/10 cases in the neocortex and in 6/24 cases in the hippocampus, and increased after depression in 4/8 cases in the neocortex. These latency changes could not be attributed to changes in presynaptic fibre excitability, monosynaptic inhibition, release kinetics or activation kinetics of postsynaptic ion channels. We conclude therefore that potentiation led to the activation of previously silent synapses of fast-conducting afferents and depression to the inactivation of previously functional synapses. Thus, neocortical and hippocampal synapses can be in a non-functional state, and regimes that induce long-term potentiation and depression not only change the efficacy of synapses but also alter their functional state.
在大鼠新皮层切片和豚鼠海马体中，观察到小兴奋性突触后电位潜伏期的变化与突触传递长期修饰的诱导相关。在增强后，新皮层中3/10的案例以及海马体中6/24的案例中反应潜伏期缩短，而在新皮层中4/8的案例在抑制后潜伏期延长。这些潜伏期变化不能归因于突触前纤维兴奋性、单突触抑制、释放动力学或突触后离子通道激活动力学的变化。因此，我们得出结论，增强导致快速传导传入纤维中先前沉默突触的激活，而抑制导致先前功能性突触的失活。因此，新皮层和海马体突触可以处于无功能状态，诱导长期增强和抑制的机制不仅会改变突触的效能，还会改变其功能状态。
