Facilitation of glutamate release by ionotropic glutamate receptors in osteoblasts

Eiichi Hinoi, Sayumi Fujimori, Takeshi Takarada, Hideo Taniura, Yukio Yoneda

Research output: Contribution to journalArticlepeer-review

52 Citations (Scopus)


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 Ca2+ 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.

Original languageEnglish
Pages (from-to)452-458
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - 2002
Externally publishedYes


  • AMPA receptors
  • BNPI
  • Exocytosis
  • Glutamate
  • Osteoblasts
  • Release
  • Vesicular transporter

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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