2015 Fiscal Year Final Research Report
Time-dependent Changes of PFDN5 Expression during a Long-term Potentiation-like Facilitation in Adult Mouse Hippocampus Induced by Nicotine Application
| Project/Area Number |
25860196
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Himeji Dokkyo University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | シナプス可塑性 / プレフォルディン / ニコチン |
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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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| Free Research Field |
神経薬理学
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