Chronic exposure of NG108-15 cells to amyloid beta peptide (A beta(1-42)) abolishes calcium influx via N-type calcium channels

0142217 - FGU-C 20010276 RIV US eng J - Journal Article
Kašparová, Jana - Lisá, Věra - Tuček, Stanislav - Doležal, Vladimír
Chronic exposure of NG108-15 cells to amyloid beta peptide (A beta(1-42)) abolishes calcium influx via N-type calcium channels.
Neurochemical Research. Roč. 26, 8-9 (2001), s. 1079-1084. ISSN 0364-3190. E-ISSN 1573-6903
R&D Projects: GA MZd NF5183
Institutional research plan: CEZ:AV0Z5011922
Keywords : amyloid beta peptide * Alzheimer's disease * calcium
Subject RIV: FH - Neurology
Impact factor: 1.638, year: 2001

We investigated whether amyloid-peptide (A1-42) 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. A1-42 (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 A1-42. Nifedipine (1 microM) reduced these elevations equally in cells grown in the absence or presence of A1-42. In contrast, the ability of ?-conotoxin GVIA to diminish the depolarization-induced [Ca2+]i responses became lost in cells grown in the presence of 100 nM A1-42. 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 A1-42 , 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.
Permanent Link: http://hdl.handle.net/11104/0039924