Depolarization of human neuroblastoma cells as a result of muscarinic receptor‐induced rise in cytosolic Ca2+

FEBS Letters

Åkerman, Karl E.O.¹ 

[1] Department of Biochemistry and Pharmacy, Åbo Akademi, SF-20500 Turku, Finland

关键词: Muscarinic receptor;    Depolarization;    Carbachol;    Fura-2;    Bisoxonol;    Ca2+;    Na+;    BAPTA/AM;    1;    2-bis(o-aminophenoxy)-ethane N;    N;    N′;    N′-tetraacetic acid acetoxymethylester;    fura-2/AM;    fura-2-acetoxymethylester;    H-EDTA;    N-hydroxyethylene-diamine triacetic acid;    TPA;    12-O-tetradecanoyl-phorbol-13-acetate;    Tes;    2-{[2-hydroxy-1;    1-bis(hydroxymethyl)ethyl]amino}-ethanesulphonic acid;    PBS;    phosphate-buffered saline;   

DOI  :  10.1016/0014-5793(89)80497-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The role of intracellular free Ca²⁺ in muscarinic-receptor linked depolarization of SH-SY5Y neuroblastoma cells has been determined by using the bisoxonol membrane potential probe DiBaC₄−(3) and intracellular Ca²⁺ indicator fura-2-respectively. Carbachol and the Ca²⁺ ionophore, ionomycin, at concentrations which caused similar rises in intracellular Ca²⁺ increased the bisoxonol fluorescence (depolarization) to the same extent. The membrane potential responses, but not the changes in intracellular Ca²⁺, were dependent on extracellular Na⁺. Ionomycin depletion of intracellular Ca²⁺ with EGTA and ionomycin or loading the cells with a Ca²⁺ buffer, BAPTA, reduced the carbachol-induced depolarization. The results suggest that a rise in intracellular Ca²⁺ may cause depolarization through an increase in the Na⁺ permeability.

【 授权许可】

Unknown