Počet záznamů: 1  

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

  1. 1. 0142217 - FGU-C 20010276 RIV US eng J - Článek v odborném periodiku
    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
    Grant CEP: GA MZd NF5183
    Výzkumný záměr: CEZ:AV0Z5011922
    Klíčová slova: amyloid beta peptide * Alzheimer's disease * calcium
    Kód oboru RIV: FH - Neurologie, neurochirurgie, neurovědy
    Impakt faktor: 1.638, rok: 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.
    Trvalý link: http://hdl.handle.net/11104/0039924