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The Journal of Neuroscience, January 23, 2008, 28(4):843-849; doi:10.1523/JNEUROSCI.4397-07.2008

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Development/Plasticity/Repair
Neuropsin (KLK8)-Dependent and -Independent Synaptic Tagging in the Schaffer-Collateral Pathway of Mouse Hippocampus

Yasuyuki Ishikawa,^1,2 Yoichiro Horii,¹ Hideki Tamura,^1,2 and Sadao Shiosaka^1,2

¹Division of Structural Cell Biology, Nara Institute of Science and Technology, Ikoma, Nara 630-0192, Japan, and ²Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Ikoma, Nara 630-0192, Japan

Correspondence should be addressed to Dr. Sadao Shiosaka, Division of Structural Cell Biology, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara 630-0192, Japan. Email: sshiosak{at}bs.naist.jp

Hippocampal early long-term potentiation (LTP) elicited by a weak (one or two) tetanic stimulus normally fades away within 90 min. 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 (i.e., 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 Ca²⁺ 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 nonstressful associative memory.

Key words: kallikrein-related peptidase 8; extracellular proteolysis; LTP (long-term potentiation); synaptic capture; synaptic plasticity; integrin

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Received Sept. 26, 2007; revised Dec. 5, 2007; accepted Dec. 10, 2007.

Correspondence should be addressed to Dr. Sadao Shiosaka, Division of Structural Cell Biology, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara 630-0192, Japan. Email: sshiosak{at}bs.naist.jp

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