DISSECTION OF BRADYKININ-EVOKED RESPONSES BY BUFFERING INTRACELLULAR CA2+ IN NEUROBLASTOMA X GLIOMA HYBRID NG108-15 CELLS

被引:15
作者
KIMURA, Y [1 ]
HIGASHIDA, H [1 ]
机构
[1] KANAZAWA UNIV,SCH MED,NEUROINFORMAT RES INST,DEPT BIOPHYS,13-1 TAKARA MACHI,KANAZAWA,ISHIKAWA 920,JAPAN
关键词
BRADYKININ; CA2+ CHELATOR; INOSITOL TRISPHOSPHATE; INTRACELLULAR CA2+; K+ CURRENTS; ACETYLCHOLINE RELEASE; NEUROBLASTOMA HYBRID CELLS;
D O I
10.1016/0168-0102(92)90007-Y
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Signal transduction pathways from bradykinin (BK) receptors were investigated in NG108-15 neuroblastoma X glioma hybrid cells by buffering the intracellular calcium (Ca2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a Ca2+ chelator. BK increased inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) formation at the same rate in the control and in BAPTA-acetoxy methyl ester (AM)-treated NG108-15 cells. However, a transient increase of intracellular Ca2+ concentrations in response to BK was significantly suppressed in Ca2+-buffered hybrid cells. Accordingly the BK-induced outward current was inhibited in BAPTA-AM-treated hybrid cells, while the subsequent inward current associated with a fall in membrane conductance was apparently increased. The initial phase of acetylcholine release from NG108-15 cells in response to BK was markedly inhibited in BAPTA-AM-treated coculture dishes when detected as miniature end-plate potentials of myotubes, though the late phase of acetylcholine secretion was observed. These results indicate that BK induces two distinct responses in NG108-15 cells: Ins(1,4,5)P3-dependent intracellular Ca2+ rise-sensitive and -insensitive components.
引用
收藏
页码:213 / 220
页数:8
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