ArticleNeurochemical research2001
Chronic exposure of NG108-15 cells to amyloid beta peptide (A beta(1-42)) abolishes calcium influx via N-type calcium channels.
Article in Neurochemical research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Reduction of Dendritic Inhibition in CA1 Pyramidal Neurons in Amyloidosis Models of Early Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2020Article
- Calcium channel blockers and dementia.British journal of pharmacology · 2013Review
- The increase of choline acetyltransferase activity by docosahexaenoic acid in NG108-15 cells grown in serum-free medium is independent of its effect on cell growth.Neurochemical research · 2006Article
- Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress.Neurochemical research · 2004Review
- Beta-amyloid and cholinergic neurons.Neurochemical research · 2003Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated whether amyloid-beta-peptide (A beta(1-42)) has an effect on the elevations of the intracellular concentration of Ca2+ ions ([Ca2+]i) induced by depolarizations of NG108-15 cells and on related Ca2+ channels. A beta(1-42) (10-1000 nM) had no immediate effect on depolarization-induced [Ca2+]i elevations. [Ca2+]i increases were slightly diminished in cells grown in the presence of 100 or 1000 nM A beta(1-42). Nifedipine (1 microM) reduced these elevations equally in cells grown in the absence or presence of A beta(1-42). In contrast, the ability of omega-conotoxin GVIA to diminish the depolarization-induced [Ca2+]i responses became lost in cells grown in the presence of 100 nM A beta(1-42). This indicates that the influx of calcium through the N-type Ca2+ channels was compromised by the chronic exposure of cells to a submicromolar concentration of A beta(1-42), presumably because of impairement of their function or diminished expression. This may be important in the pathogeny of Alzheimer's dementia in view of the pivotal role of N-type Ca2+ channels in neurotransmitter release.
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