Abstract
Although the mechanisms of Ca2+ wave propagation in astrocytes induced by mechanical stimulation have been well studied, it is still not known how the [Ca2+]i increases in the stimulated cells. Here, we have analyzed the mechanisms of [Ca2+]i increase in single, isolated astrocytes. Our results showed that there was an autocrine mechanism of Ca2+ regulation mediated by ATP in mechanically stimulated astrocytes. This autocrine mechanism induced the activation of phospholipase C via a G-protein, resulting in Ca2+ release from intracellular Ca2+ stores. A second pathway mediating a [Ca2+]i increase was via a Ca2+ influx from the extracellular space, which, interestingly, suppressed an intracellular Ca2+ oscillation. These two different Ca2+ cascades are involved in signal transduction and may function separately during intercellular communication.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / metabolism*
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Animals
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Astrocytes / cytology
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Astrocytes / drug effects
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Astrocytes / metabolism*
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Autocrine Communication / drug effects
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Autocrine Communication / physiology*
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Calcium / metabolism
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Calcium Signaling / drug effects
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Calcium Signaling / physiology*
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Cells, Cultured
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Estrenes / pharmacology
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GTP-Binding Proteins / metabolism
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Intracellular Fluid / metabolism
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Phosphodiesterase Inhibitors / pharmacology
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Physical Stimulation
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Purinergic P2 Receptor Antagonists
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Pyrrolidinones / pharmacology
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Rats
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Rats, Wistar
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Suramin / pharmacology
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Type C Phospholipases / antagonists & inhibitors
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Type C Phospholipases / metabolism
Substances
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Estrenes
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Phosphodiesterase Inhibitors
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Purinergic P2 Receptor Antagonists
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Pyrrolidinones
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1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione
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Suramin
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Adenosine Triphosphate
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Type C Phospholipases
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GTP-Binding Proteins
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Calcium