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Cooling sensitive [Ca] response associated with signaling of G protein-coupled receptors
The influence of cooling on the intracellular concentration of Ca super(2+) ([Ca super(2+)] sub(i)) was tested in cell lines expressing chemical receptors. First, when ATP was externally added to rat basophilic leukemia (RBL-2H3) cells, cooling from 37 degree C to 27 degree C induced a transient rap...
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Published in: | Biochemical and biophysical research communications 1998-07, Vol.248 (3), p.733-737 |
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description | The influence of cooling on the intracellular concentration of Ca super(2+) ([Ca super(2+)] sub(i)) was tested in cell lines expressing chemical receptors. First, when ATP was externally added to rat basophilic leukemia (RBL-2H3) cells, cooling from 37 degree C to 27 degree C induced a transient rapid increase in [Ca super(2+)] sub(i). In the absence of extracellular Ca super(2+), the [Ca super(2+)] sub(i) response was induced whereas an inhibitor of microsomal Ca super(2+) ATPase, thapsigargin, largely abolished the [Ca super(2+)] sub(i) response, suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). A purinergic receptor antagonist, suramin, completely inhibited the [Ca super(2+)] sub(i) response to the cooling. Secondly, when serotonin (5-HT) was added to rat glioma C6BU-1 cells, the cooling induced a transient increase in [Ca super(2+)] sub(i). This [Ca super(2+)] sub(i) response was induced in the absence of external Ca super(2+), suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). These results raise the possibility that some G protein-coupled receptors are sensitive to cooling in the presence of agonist for the receptor. |
doi_str_mv | 10.1006/bbrc.1998.8873 |
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First, when ATP was externally added to rat basophilic leukemia (RBL-2H3) cells, cooling from 37 degree C to 27 degree C induced a transient rapid increase in [Ca super(2+)] sub(i). In the absence of extracellular Ca super(2+), the [Ca super(2+)] sub(i) response was induced whereas an inhibitor of microsomal Ca super(2+) ATPase, thapsigargin, largely abolished the [Ca super(2+)] sub(i) response, suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). A purinergic receptor antagonist, suramin, completely inhibited the [Ca super(2+)] sub(i) response to the cooling. Secondly, when serotonin (5-HT) was added to rat glioma C6BU-1 cells, the cooling induced a transient increase in [Ca super(2+)] sub(i). This [Ca super(2+)] sub(i) response was induced in the absence of external Ca super(2+), suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). 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First, when ATP was externally added to rat basophilic leukemia (RBL-2H3) cells, cooling from 37 degree C to 27 degree C induced a transient rapid increase in [Ca super(2+)] sub(i). In the absence of extracellular Ca super(2+), the [Ca super(2+)] sub(i) response was induced whereas an inhibitor of microsomal Ca super(2+) ATPase, thapsigargin, largely abolished the [Ca super(2+)] sub(i) response, suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). A purinergic receptor antagonist, suramin, completely inhibited the [Ca super(2+)] sub(i) response to the cooling. Secondly, when serotonin (5-HT) was added to rat glioma C6BU-1 cells, the cooling induced a transient increase in [Ca super(2+)] sub(i). This [Ca super(2+)] sub(i) response was induced in the absence of external Ca super(2+), suggesting that the internal Ca super(2+) stores liberate the Ca super(2+). These results raise the possibility that some G protein-coupled receptors are sensitive to cooling in the presence of agonist for the receptor.</abstract><doi>10.1006/bbrc.1998.8873</doi><tpages>5</tpages></addata></record> |
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title | Cooling sensitive [Ca] response associated with signaling of G protein-coupled receptors |
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