Depolarization of human neuroblastoma cells as a result of muscarinic receptor-induced rise in cytosolic Ca2+.
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.
Akerman
K E
KE
Department of Biochemistry and Pharmacy, Abo Akademi, Turku, Finland.
D002118:Calcium / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology; D003600:Cytosol / Q000502:physiology; D004987:Ethers / Q000494:pharmacology; D006801:Humans; D015759:Ionomycin; D008564:Membrane Potentials / Q000187:drug effects; D009447:Neuroblastoma / Q000503:physiopathology*; D011976:Receptors, Muscarinic / Q000502:physiology*; D012964:Sodium / Q000502:physiology; D014407:Tumor Cells, Cultured
D004987:Ethers; D011976:Receptors, Muscarinic; D015759:Ionomycin; D002217:Carbachol; D012964:Sodium; D002118:Calcium