Capacitative Ca2+ influx in glial cells is inhibited by glycolytic inhibitors.

Abstract:

:In non-excitable cells, stimulation of phosphoinositide (PI) turnover and inhibition of the endoplasmic reticulum (ER) Ca2+-ATPase are methods commonly used to deplete calcium stores, resulting in a capacitative Ca2+ influx (i.e., Ca2+ release-activated Ca2+ influx). Since this Ca2+ influx in glial cells has not been thoroughly investigated, we have used C6 glioma cells as a glial cell model to study this phenomenon. On adding cyclopiazonic acid (CPA) or thapsigargin (TG) (two ER Ca2+-ATPase inhibitors) in Ca2+-free medium, only a small transient increase in intracellular Ca2+ was seen. After depletion of the stored Ca2+, a marked Ca2+ influx, followed by a prolonged plateau, was seen on re-addition of extracellular Ca2+ ions (2 mM), i.e., capacitative Ca2+ influx. A similar effect was seen on adding ATP, known to deplete the inositol triphosphate (IP3)-sensitive Ca2+ store in C6 cells. After various degrees of store depletion, the amplitude of the capacitative Ca2+ influx was found to be highly dependent on the amount of Ca2+ remaining in the store. This Ca2+ influx was markedly inhibited by (1) La3+ and Ni2+, (2) SK&F 96365, econazole, and miconazole, and (3) membrane depolarization, clearly showing that this Ca2+ influx after store depletion in C6 cells is a capacitative mechanism. Interestingly, the capacitative Ca2+ influx can be inhibited by a reduction in intracellular ATP (ATPi) levels in glial cells. The role of ATPi in the capacitative Ca2+ influx is discussed.

journal_name

Glia

journal_title

Glia

authors

Wu ML,Kao EF,Liu IH,Wang BS,Lin-Shiau SY

doi

10.1002/(sici)1098-1136(199711)21:3<315::aid-glia6

subject

Has Abstract

pub_date

1997-11-01 00:00:00

pages

315-26

issue

3

eissn

0894-1491

issn

1098-1136

pii

10.1002/(SICI)1098-1136(199711)21:3<315::AID-GLIA6

journal_volume

21

pub_type

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