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Predominant loss of glutamatergic terminal markers in a β-amyloid peptide model of alzheimer's disease.
MedLine Citation:
PMID:  24029236     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Alzheimer's disease (AD) is characterized phenotipically by memory impairment, neurochemically by accumulation of β-amyloid peptide (such as Aβ1-42) and morphologically by an initial loss of nerve terminals in cortical and hippocampal regions. However, it is not known what nerve terminals are mostly affected in early AD. We now used a mouse model of AD, based on the intra-cerebral administration of soluble Aβ1-42, that leads to memory impairment and loss of nerve terminal markers within 2 weeks, to investigate which type of hippocampal nerve terminals was mostly affected in the hippocampus. Western blot analysis revealed a decrease of the density of vesicular glutamate transporters type 1 (vGluT1, a marker of glutamatergic terminals; -20.1±3.6%) and of vesicular acetylcholine transporters (vAChT, a marker of cholinergic terminals; -27.2±0.9%) but not of vesicular GABA transporters (vGAT, a marker of GABAergic terminals) in the hippocampus of Aβ-injected mice. Immunocytochemical analysis of single hippocampal nerve terminals revealed that the decrease of the density of vGluT1 reflects a reduction of the number of vGluT1-immunopositive nerve terminals (-10.6±3.6%), while no significant changes in the number of vAChT- or vGAT-immunopositive nerve terminals were observed. This pilot study shows that, in this Aβ-based model of AD, there is an asymmetric loss of different synaptic markers with a predominant susceptibility of glutamatergic synapses.
Authors:
Paula M Canas; Ana Patrícia Simões; Ricardo J Rodrigues; Rodrigo A Cunha
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-9-9
Journal Detail:
Title:  Neuropharmacology     Volume:  -     ISSN:  1873-7064     ISO Abbreviation:  Neuropharmacology     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-9-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2013 Published by Elsevier Ltd.
Affiliation:
CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
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