Abstract
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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