| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
Long-lasting synaptic plasticity requires changes of protein expression, although the mechanisms remain unclear. We previously reported that nicotine expressed a long-term potentiation-like facilitation, that is synaptic plasticity, in mouse hippocampus. In this study, we conducted to clarify the involvement of Prefoldin subunit 5 (PFDN5) in synaptic plasticity.After nicotine treatment (3 mg/kg, i.p.), mRNA and protein expression of PFDN5 in hippocampus increased gradually during 2-24-hr period. This enhanced expression of PFDN5 protein at 24-hr was not completely inhibited by pretreatment of mecamylamine (0.5 mg/kg, i.p.), a nonselective nicotinic ACh receptor (nAChR) antagonist. Ubiquitinated PFDN5 increased during synaptic plasticity after nicotine treatment.These findings demonstrated that PFDN5 protein was enhanced during synaptic plasticity through coordinated regulation of gene expression and protein degradation.
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