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    Modulation of astroglial glutamate receptors by epidermal growth factor

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    https://www.riss.kr/link?id=E685609

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    We attempted to elucidate factors which can modulate astroglial glutamare receptors. Glutamate induced two phases of intracellular calcium(Ca^2+i) increase in astrocytes: rapid, large, and short increase followed by relatively slow, small and long-lasting increase (Cornell-Bell et al.,1990). Pretreatment of cpidcrmal growth factor(EGF, 10ng/ml), 5·10 minutes prior to glutamate, abolished or significantly reduced both phases of Ca^2+i increase. Similar result were obtained with an agonist of metabotropic receptor, aminocyclopently dicarboxylic acid (ACPD). In contrary to EGF, basic fibrobiast growth factor (bFGF) did not produce such effect. The effect of EGF seems to be specific to Ca^2+i increase due to the activation of glutamate receptors because EGF had no effect on Ca^2+i increase induced by either activation of ATP receptors or high potassium. The modulatory effect of EGF on astroglial glutamate receptors was completely inhibited by lavendustin A, a membrane permeable tyrosine kinase (TK) inhibitor. These results suggest that EGF directly modulate astroglial glutamate receptors via TK activity which might be a specific function of EGF.
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    We attempted to elucidate factors which can modulate astroglial glutamare receptors. Glutamate induced two phases of intracellular calcium(Ca^2+i) increase in astrocytes: rapid, large, and short increase followed by relatively slow, small and long-la...

    We attempted to elucidate factors which can modulate astroglial glutamare receptors. Glutamate induced two phases of intracellular calcium(Ca^2+i) increase in astrocytes: rapid, large, and short increase followed by relatively slow, small and long-lasting increase (Cornell-Bell et al.,1990). Pretreatment of cpidcrmal growth factor(EGF, 10ng/ml), 5·10 minutes prior to glutamate, abolished or significantly reduced both phases of Ca^2+i increase. Similar result were obtained with an agonist of metabotropic receptor, aminocyclopently dicarboxylic acid (ACPD). In contrary to EGF, basic fibrobiast growth factor (bFGF) did not produce such effect. The effect of EGF seems to be specific to Ca^2+i increase due to the activation of glutamate receptors because EGF had no effect on Ca^2+i increase induced by either activation of ATP receptors or high potassium. The modulatory effect of EGF on astroglial glutamate receptors was completely inhibited by lavendustin A, a membrane permeable tyrosine kinase (TK) inhibitor. These results suggest that EGF directly modulate astroglial glutamate receptors via TK activity which might be a specific function of EGF.

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    목차 (Table of Contents)

    • Abstract
    • Introduction
    • Abstract
    • Introduction
    • Materials and Methods
    • Discussion
    • References
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