Long-term activation of capacitative Ca2+ entry in mouse microglial cells
In: Neuroscience, Jg. 86 (1998), Heft 3, S. 925-935
academicJournal
- print, 41 ref
Zugriff:
The cytoplasmic free calcium concentration ([Ca2+]i) was measured in cultured microglial cells with the Ca2+-sensitive fluorescent dye Fura-2 using a digital imaging system. Stimulation of P2 purinergic receptors by ATP or UTP always evoked a [Ca2+]i elevation. The ATP-induced Ca2+ response involved both Ca2+ influx through ionotropic receptors and Ca2+ release from intracellular pools. whereas UTP selectively stimulated intracellular Ca2+ release. When intracellular Ca2+ release was stimulated in the absence of extracellular Ca2+, the readmission of extracellular Ca2+ caused a large rebound [Ca2+]i increase. Following this rebound, [Ca2+]i did not return to the initial resting level. but remained for long periods of time (up to 20 min), at a new. higher steady-state level. Both the amplitude of the rebound Ca2+ transient and the new plateau level strongly correlated with the degree of intracellular Ca2+ depletion. indicating the activation of a store-operated Ca2+ entry pathway. The elevated steady-state [Ca2+]i level was associated with a significant increase in the plasma membrane permeability to Ca2+. as changes in extracellular Ca2+ were reflected in almost immediate changes of [Ca2+]i. Similarly. blocking plasma-lemmal Ca2+ channels with the non-specific agonist La3+ (50 μM) caused a decrease in [Ca2+]i. despite the continuous presence of Ca2+ ions in the extracellular medium. After the establishment of the new. elevated steady-state [Ca2+]i level. stimulation of P21 metabotropic purinoreceptors did not induce a [Ca2+]i response. In addition, application of either thapsigargin (1 μM) or carbonyl cyanide chlorophenyl hydrazone (10 μM) failed to affect [Ca2+]i. We conclude that the maximal depletion of intracellular Ca2+ stores in mouse brain microglia determines the long-term activation of plasma membrane Ca2+ entry pathway. This activation appears to be associated with a significant decrease in the capability of the intracellular Ca2+ stores to take up cytosolic Ca2+ once they have been maximally depleted.
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Long-term activation of capacitative Ca2+ entry in mouse microglial cells
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Autor/in / Beteiligte Person: | TOESCU, E. C ; MÖLLER, T ; KETTENMANN, H ; VERKHRATSKY, A |
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Zeitschrift: | Neuroscience, Jg. 86 (1998), Heft 3, S. 925-935 |
Veröffentlichung: | Oxford: Elsevier, 1998 |
Medientyp: | academicJournal |
Umfang: | print, 41 ref |
ISSN: | 0306-4522 (print) |
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