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

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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.