Facilitation of glutamate release by ionotropic glutamate receptors in osteoblasts
Constitutive expression of mRNA was seen for the vesicular glutamate transporter brain-specific Na +-dependent inorganic phosphate cotransporter (BNPI), but not differentiation-associated Na +-dependent inorganic phosphate cotransporter, in rat calvarial osteoblasts cultured for 7 and 21 days in vit...
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Published in | Biochemical and biophysical research communications Vol. 297; no. 3; pp. 452 - 458 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
27.09.2002
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Subjects | |
Online Access | Get full text |
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Summary: | Constitutive expression of mRNA was seen for the vesicular glutamate transporter brain-specific Na
+-dependent inorganic phosphate cotransporter (BNPI), but not differentiation-associated Na
+-dependent inorganic phosphate cotransporter, in rat calvarial osteoblasts cultured for 7 and 21 days in vitro (DIV). Three different agonists for ionotropic glutamate receptors (iGluR) at 1
mM, as well as 50
mM KCl, significantly increased the release of endogenous
l-glutamate from osteoblasts cultured for 7
DIV when determined 5
min after the addition by using a high performance liquid chromatograph. The inhibitor of desensitization of
dl-α-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA) receptors cyclothiazide significantly potentiated and prolonged the release of endogenous
l-glutamate evoked by AMPA in a dose-dependent manner. The release evoked by AMPA was significantly prevented by the addition of an AMPA receptor antagonist as well as by the removal of Ca
2+ ions. These results suggest that endogenous
l-glutamate could be released from intracellular vesicular constituents associated with BNPI through activation of particular iGluR subtypes expressed in cultured rat calvarial osteoblasts. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/S0006-291X(02)02223-4 |