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Depolarization of human neuroblastoma cells as a result of muscarinic receptor‐induced rise in cytosolic Ca 2+
Author(s) -
Åkerman Karl E.O.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80497-1
Subject(s) - ionomycin , depolarization , intracellular , fura 2 , biophysics , extracellular , egta , chemistry , carbachol , membrane potential , bapta , muscarinic acetylcholine receptor , cytosol , biology , calcium , biochemistry , receptor , organic chemistry , enzyme
The role of intracellular free Ca 2+ in muscarinic‐receptor linked depolarization of SH‐SY5Y neuroblastoma cells has been determined by using the bisoxonol membrane potential probe DiBaC 4 −(3) and intracellular Ca 2+ indicator fura‐2‐respectively. Carbachol and the Ca 2+ ionophore, ionomycin, at concentrations which caused similar rises in intracellular Ca 2+ increased the bisoxonol fluorescence (depolarization) to the same extent. The membrane potential responses, but not the changes in intracellular Ca 2+ , were dependent on extracellular Na + . Ionomycin depletion of intracellular Ca 2+ with EGTA and ionomycin or loading the cells with a Ca 2+ buffer, BAPTA, reduced the carbachol‐induced depolarization. The results suggest that a rise in intracellular Ca 2+ may cause depolarization through an increase in the Na + permeability.