Stimulation of calcium uptake in cultured astrocytes by hypoosmotic stress — effect of cyclic AMP
Identifieur interne : 001000 ( Main/Exploration ); précédent : 000F99; suivant : 001001Stimulation of calcium uptake in cultured astrocytes by hypoosmotic stress — effect of cyclic AMP
Auteurs : Alex S. Bender [États-Unis] ; Lily L. Mantelle [États-Unis] ; Michael D. Norenberg [États-Unis]Source :
- Brain Research [ 0006-8993 ] ; 1994.
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Abstract
Abstract: To investigate the role of Ca2+ in astrocyte volume regulation, we determined Ca2+ fluxes following hypoosmotic stress and how these fluxes were modified by cyclic AMP. In isoosmotic conditions treatment with dibutyryl cyclic AMP (dBcAMP) caused almost a twofold increase in 45Ca2+ uptake. Efflux studies of 45Ca2+ in dBcAMP-treated cells showed three Ca2+ compartments while only two Ca2+ compartments were identified in non-dBcAMP-treated cells. Following hypoosmotic stress a twofold stimulation of 45Ca2+ uptake occurred in both non-dBcAMP-treated and dBcAMP-treated astrocytes. Stimulation of Ca2+ uptake begins at ∼ 270 mOsm and is half-maximally stimulated at ∼ 100 mOsm. This uptake is partly mediated through L-type ‘slow’ inactivating Ca2+ channels. Hypoosmotic stress also induces the release of Ca2+ from intracellular stores. The influx of extracellular Ca2+ and efflux of intracellular Ca2+ appear to be important factors in volume regulation after hypoosmotic stress. Cyclic AMP plays an important role in modulating hypoosmotically stimulated Ca2+ uptake.
Url:
DOI: 10.1016/0006-8993(94)91634-9
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In isoosmotic conditions treatment with dibutyryl cyclic AMP (dBcAMP) caused almost a twofold increase in 45Ca2+ uptake. Efflux studies of 45Ca2+ in dBcAMP-treated cells showed three Ca2+ compartments while only two Ca2+ compartments were identified in non-dBcAMP-treated cells. Following hypoosmotic stress a twofold stimulation of 45Ca2+ uptake occurred in both non-dBcAMP-treated and dBcAMP-treated astrocytes. Stimulation of Ca2+ uptake begins at ∼ 270 mOsm and is half-maximally stimulated at ∼ 100 mOsm. This uptake is partly mediated through L-type ‘slow’ inactivating Ca2+ channels. Hypoosmotic stress also induces the release of Ca2+ from intracellular stores. The influx of extracellular Ca2+ and efflux of intracellular Ca2+ appear to be important factors in volume regulation after hypoosmotic stress. 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