Structural Synaptic Plasticity Integration and Conversion form Short-term into Long-term Memory

由一个或两个强直刺激引起的海马区早期长时程增强(LTP)通常在90分钟内消失。由强(四个)刺激引起的晚期LTP持续180分钟，需要新的蛋白质合成才能持续。如果将强破伤风注射到突触一次，即使是弱破伤风注射到另一个突触也能引起持久的LTP。据推测，突触标签能够捕获新合成的突触分子。在这里，我们发现了弱刺激突触获得持续性的两种突触捕获机制(即，神经蛋白素依赖和非依赖)。单次破伤风引起神经降压素依赖形式，其下游信号转导为整合素/肌动蛋白信号和L电压依赖性钙通道通路。此外，比前者更强的(两个)破伤风会诱发一种不依赖神经蛋白的突触捕获形式。这两种形式在LVDCC上的融合可能服务于不同的联想记忆，这取决于它们的输入强度。我们的研究有力地支持了突触标记的假说，并证明了神经蛋白依赖的晚期联想在非应激性联想记忆中特别重要。

Hippocampal early long-term potentiation (LTP) elicited by a weak (one or two) tetanic stimulus normally fades away within 90min. Late LTP elicited by strong (four) stimuli lasts 180 min and requires new protein synthesis to persist. If a strong tetanus is injected once into a synapse, even a weak tetanus injected into another synapse can evoke persistent LTP. It was hypothesized that a synaptic tag enables capture of newly synthesized synaptic molecules. Here, we found two synaptic capture mechanisms for a weakly stimulated synapse to acquire persistency (ie., neuropsin-dependent and -independent). The single tetanus evokes a neuropsin-dependent form that follows downstream signaling into integrin/actin signal and L-type voltage-dependent Ca^2 channel (LVDCC) pathway. Additionally, a neuropsin-independent form of synaptic capture is evoked by a stronger (two) tetanus than the former. Both forms converging on LVDCC might serve different associative memories depending on their input strength. Our study strongly supports the hypothesis of synaptic tagging and demonstrates that neuropsin-dependent late associativity is particularly important in non-stressful associative memory.