title: Appearance of depolarization- and maitotoxin-induced [Ca2+]i elevation in single LAN-1 human neuroblastoma cells on exposure to retinoic acid.
abstract: LAN-1 is a human neuroblastoma cell line that, in the undifferentiated state, does not respond to membrane depolarization with an elevation of [Ca2+]i, monitored by fura-2 single-cell microfluorimetry. The exposure of LAN-1 cells to the differentiating agent retinoic acid induced the appearance of [Ca2+]i elevation elicited by 55 mM K+. Maitotoxin, a putative activator of voltage-sensitive Ca2+ channels, did not evoke an elevation of [Ca2+]i in undifferentiated LAN-1 cells, but produced a marked and sustained increase in [Ca2+]i when superfused in retinoic acid-treated cells. Both high K(+)- and maitotoxin-induced [Ca2+]i elevation in retinoic acid-differentiated LAN-1 cells was reversed by the lanthanide Gd3+, an inorganic Ca(2+)-entry blocker, and by the snail toxin omega-conotoxin GVIA, which interacts with the N subtype of voltage-sensitive Ca2+ channels. In contrast, both Bay K 8644 and nimodipine, dihydropyridines that selectively activate or block, respectively, the L-channel subtype, were completely ineffective. The tumor promoter phorbol 12-myristate 13-acetate (100 nM), a protein kinase C activator, inhibited the elevation of [Ca2+]i due to Ca2+ influx elicited by membrane depolarization. K(+)-induced [Ca2+]i elevation appeared 24 h after the addition of retinoic acid and reached the highest magnitude after 72 h. Furthermore, 8 days after the removal of the differentiating agent from the culture medium, the high K(+)-induced increase of [Ca2+]i was still present.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neuroscience, School of Medicine, Federico II University of Naples, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Fatatis
authors.forename: A
authors.initials: A
authors.lastname: Bassi
authors.forename: E
authors.initials: E
authors.lastname: Iannotti
authors.forename: N
authors.initials: N
authors.lastname: Caso
authors.forename: G D
authors.initials: GD
authors.lastname: Mita
authors.forename: G
authors.initials: G
authors.lastname: Di Renzo
authors.forename: L
authors.initials: L
authors.lastname: Annunziato
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D002118:Calcium / Q000032:analysis / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects; D003592:Cytophotometry; D006801:Humans; D008387:Marine Toxins / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009447:Neuroblastoma / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology*; D009553:Nimodipine / Q000494:pharmacology; D035964:Oxocins; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013997:Time Factors; D014212:Tretinoin / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D020866:omega-Conotoxin GVIA; D000095702:Polyether Toxins
chemical_list: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D002118:Calcium; D008387:Marine Toxins; D009553:Nimodipine; D035964:Oxocins; D010455:Peptides; D011188:Potassium; D013755:Tetradecanoylphorbol Acetate; D014212:Tretinoin; D020866:omega-Conotoxin GVIA; C020394:maitotoxin; D000095702:Polyether Toxins