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URL Address
<a href="http://doi.org/10.1002/jnr.21035" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jnr.21035</a>
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Pages
1303-1310
Issue
6
Volume
84
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Title
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Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of Down syndrome
Publisher
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Journal of Neuroscience Research
Date
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2006
2006-11
Subject
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16 mice; abnormalities; acetylcholine; acetylcholine-release; alzheimers-disease; amyloid; antisense; beta-protein; calcium; cell line; Down syndrome; Neurosciences & Neurology; neurotoxicity; peptide; rat hippocampal slices; root ganglion neurons
Creator
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Opazo P; Saud K; de Saint Pierre M; Cardenas A M; Allen D D; Segura-Aguilar J; Caviedes R; Caviedes P
Description
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We have generated immortal neuronal cell lines from normal and trisomy 16 (Ts16) mice, a model for Down syndrome (DS). Ts16 lines overexpress DS-related genes (App, amyloid precursor protein; Sod1, Cu/Zn superoxide dismutase) and show altered cholinergic function (reduced choline uptake, ChAT expression and fractional choline release after stimulation). As previous evidence has related amyloid to cholinergic dysfunction, we reduced APP expression using specific mRNA antisense sequences in our neuronal cell line named CTb, derived from Ts16 cerebral cortex, compared to a cell line derived from a normal animal, named CNh. After transfection, Western blot studies showed APP expression knockdown in CTb cells of 36% (24 hr), 40.4% (48 hr), and 50.2% (72 hr) compared to CNh. Under these reduced APP levels, we studied 3 H-choline uptake in CTb and CNh cells. CTb, as reported previously, expressed reduced choline uptake compared to CNh cells (75%, 90%, and 69% reduction at 1, 2, and 5 min incubation, respectively). At 72 hr of APP knockdown, choline uptake levels were essentially similar in both cell types. Further, fractional release of H-3-choline in response to glutamate, nicotine, and depolarization with KCI showed a progressive increase after APP knockdown, reaching values similar to those of CNh after 72 hr of transfection. The results suggest that APP overexpression in CTb cells contributes to impaired cholinergic function, and that gene knockdown in CTb cells is a relevant tool to study DS-related dysfunction. (c) 2006 Wiley-Liss, Inc.
Identifier
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<a href="http://doi.org/10.1002/jnr.21035" target="_blank" rel="noreferrer noopener">10.1002/jnr.21035</a>
Format
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Journal Article
16 mice
2006
Abnormalities
Acetylcholine
acetylcholine-release
Allen D D
alzheimers-disease
amyloid
antisense
beta-protein
calcium
Cardenas A M
Caviedes P
Caviedes R
Cell Line
de Saint Pierre M
Down syndrome
Journal Article
Journal of neuroscience research
Neurosciences & Neurology
Neurotoxicity
Opazo P
peptide
rat hippocampal slices
root ganglion neurons
Saud K
Segura-Aguilar J