Project/Area Number |
17300118
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | Nara Institute of Science and Technology |
Principal Investigator |
SHIOSAKA Sadao Nara Institute of Science and Technology, Garduate School of Biological, Sciences, Professor (90127233)
|
Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Yasuyuki Nara Institute of Science and Technology, Graduate School of Biological Sciences, Assistant Professor (90346320)
|
Project Period (FY) |
2005 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥15,520,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥720,000)
Fiscal Year 2007: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2006: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 2005: ¥6,400,000 (Direct Cost: ¥6,400,000)
|
Keywords | Ectodomain shedding / serine protease / neuropsin / neural plasticity / learning and memory / cell adhesion molecule / Llcam / long-term potentiation / Llcam / 記憶 / L1 |
Research Abstract |
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.
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