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

由弱（一个或两个）强直刺激引起的海马早期长时程增强（LTP）通常在90分钟内消失。晚期LTP由强（四）刺激引起持续180分钟，需要新的蛋白质合成持续。如果一次强破伤风注射到一个突触中，即使是一次弱破伤风注射到另一个突触中也能引起持续的LTP。假设突触标签能够捕获新合成的突触分子。在这里，我们发现了两种突触捕获机制，用于弱刺激突触获得持久性（即，依赖性和非依赖性）。单次破伤风引起一种依赖于神经蛋白酶的形式，其下游信号传导进入整合素/肌动蛋白信号和L型电压依赖性Ca^2通道（LVDCC）通路。此外，一种不依赖于神经蛋白酶的突触捕获形式是由比前者更强的（两个）破伤风引起的。这两种形式收敛于LVDCC可能会根据其输入强度提供不同的联想记忆。我们的研究有力地支持了突触标记的假说，并证明了神经肽酶依赖的晚期关联性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.