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Appearance of Depolarization‐ and Maitotoxin‐Induced [Ca2+]i Elevation in Single LAN‐1 Human Neuroblastoma Cells on Exposure to Retinoic Acid
Journal article   Peer reviewed

Appearance of Depolarization‐ and Maitotoxin‐Induced [Ca2+]i Elevation in Single LAN‐1 Human Neuroblastoma Cells on Exposure to Retinoic Acid

Alessandro Fatatis, Antonella Bassi, Elodia Iannotti, Nino Caso, Gustavo D Mita, Gianfranco Di Renzo and Lucio Annunziato
Journal of neurochemistry, v 63(5), pp 1900-1907
Nov 1994
DOI: https://doi.org/10.1046/j.1471-4159.1994.63051900.x
PMID: 7523602
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

LAN‐1 cells Human neuroblastoma Retinoic acid Maitotoxin Voltage‐sensitive Ca2+ channels
: 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 Ca2+‐entry blocker, and by the snail toxin ω‐conotoxin GVIA, which interacts with the N sub‐type of voltage‐sensitive Ca2+ channels. In contrast, both Bay K 8644 and nimodipine, dihydropyridines that selectively activate or block, respectively, the L‐channel sub‐type, 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. In conclusion, the results of the present study demonstrated that retinoic acid‐induced differentiation of LAN‐1 cells, which lack a high K+‐evoked [Ca2+]i increase in the undifferentiated state, induces the functional expression of an ω‐conotoxin GVIA‐sensitive, dihydropyridine‐insensitive N‐type voltage‐sensitive Ca2+ channel that can be activated by maitotoxin and negatively modulated by protein kinase C.

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Web of Science research areas
Biochemistry & Molecular Biology
Neurosciences
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