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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F01%3A20010276" target="_blank" >RIV/67985823:_____/01:20010276 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

We investigated whether amyloid- -peptide (A 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 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 1-42. Nifedipine (1 M) reduced these elevations equally in cells grown in the absence or presence of A 1-42. 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 A 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 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

Název v anglickém jazyce

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

Popis výsledku anglicky

We investigated whether amyloid- -peptide (A 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 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 1-42. Nifedipine (1 M) reduced these elevations equally in cells grown in the absence or presence of A 1-42. 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 A 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 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

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FH - Neurologie, neurochirurgie, neurovědy

OECD FORD obor

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Projekt

<a href="/cs/project/NF5183" target="_blank" >NF5183: Zásahy beta-amyloidu do funkce cholinergních synapsí.</a><br>

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2001

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Neurochemical Research

ISSN

0364-3190

e-ISSN

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Svazek periodika

26

Číslo periodika v rámci svazku

8-9

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

6

Strana od-do

1079-1084

Kód UT WoS článku

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EID výsledku v databázi Scopus

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