Abstract：
:Prefoldin is a molecular chaperone that assists the folding of newly synthesized polypeptide chains and prevents aggregation of misfolded proteins. Dysfunction of prefoldin is one of the causes of neurodegenerative diseases such as Alzheimer's disease. The aim of this study was to clarify the involvement of prefoldin subunit 5 (PFDN5) in synaptic plasticity. PFDN5 protein expressed in the hippocampus was predominantly localized in the pyramidal cell layer of CA1-CA3 regions. Nicotine application caused a long-term potentiation (LTP)-like facilitation in vivo, that is synaptic plasticity, in the mouse hippocampus. The levels of PFDN5 mRNA and protein were increased 2-24 h and 4-24 h, respectively, after intraperitoneal application of nicotine (3 mg/kg, i.p.), finally returning to the basal level. This increase of PFDN5 protein was significantly inhibited by mecamylamine (0.5 mg/kg, i.p.), a non-selective nicotinic acetylcholine receptors (nAChRs) antagonist, and required combined application of ABT-418 (10 mg/kg, i.p.), a selective α4β2 nAChR agonist, and choline (30 mg/kg, i.p.), a selective α7 nAChR agonist. In transgenic mice overexpressing human tau with N279 K mutation as a model of Alzheimer's disease that showed impaired synaptic plasticity, the levels of PFDN5 mRNA and protein in the hippocampus were significantly decreased in an age-dependent manner as compared with age-matched control. The findings demonstrated that the level of PFDN5 protein in the hippocampus was changed depending on the situation of synaptic plasticity. We propose that PFDN5 could be one of the important components of synaptic plasticity.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Kadoyama K,Matsuura K,Takano M,Maekura K,Inoue Y,Matsuyama Sdoi
10.1016/j.neulet.2019.134484subject
Has Abstractpub_date
2019-11-01 00:00:00pages
134484eissn
0304-3940issn
1872-7972pii
S0304-3940(19)30587-7journal_volume
712pub_type
杂志文章abstract：:Evidence from mammalian studies suggests that brain derived neurotrophic factor (BDNF) and its receptor, trk B, are upregulated in neuronal cell bodies after injury. Although fish possess neurotrophins and display rapid functional and morphological recovery after central nervous system (CNS) injury, to date few studie...
journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
pub_type： 杂志文章
doi：10.1016/j.neulet.2009.08.043
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
pub_type： 杂志文章
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更新日期：2008-06-13 00:00:00
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journal_title：Neuroscience letters
pub_type： 杂志文章
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更新日期：2001-07-27 00:00:00
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journal_title：Neuroscience letters
pub_type： 杂志文章
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更新日期：1997-10-24 00:00:00
