title: Induction of K-channel expression in a neuroblastoma cell line.
abstract: Whole-cell currents were examined in mouse neuroblastoma cells of the N2AB-1 line. In standard culture medium, N2AB-1 cells exhibited large voltage-dependent Na currents but no discernible K currents. Treatment of N2AB-1 cells with either dimethylsulfoxide (DMSO) in low-serum medium or with retinoic acid (RA) caused the expression of delayed rectifier K currents. Currents from two types of K channel with single channel slope conductances of 15.0 pS and 6.4 pS were observed in outside-out patches from cells of both treatment groups. Thus, while N2AB-1 cells did not exhibit K currents under standard culture conditions, they did possess the gene(s) encoding K channels. The treatments caused other changes that were not directly linked to K-channel expression. RA treatment caused neurite extension in most, but not all, N2AB-1 cells; however, all RA-treated cells, including those without neurites, expressed K currents. RA treatment did not suppress cell division or cause hypertrophy. In contrast, treatment with DMSO/low serum suppressed cell division and caused cellular hypertrophy, but did not cause long neurites to form. Thus, the regulation of K channels was not coupled in a simple fashion to properties that have been associated with a differentiated neuronal phenotype: neurite elaboration, changes in cell size, and inhibition of cell division. These results suggest that N2AB-1 cells may be a good model system for investigating the processes regulating K-channel expression.
authors.affiliation: Department of Physiology, University of Rochester Medical Center, New York 14642.
authors.forename: C J
authors.initials: CJ
authors.lastname: Smith-Maxwell
authors.forename: R A
authors.initials: RA
authors.lastname: Eatock
authors.forename: T
authors.initials: T
authors.lastname: Begenisich
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D015870:Gene Expression; D008566:Membranes / Q000378:metabolism; D051379:Mice; D009423:Nervous System Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000648:ultrastructure; D009447:Neuroblastoma / Q000235:genetics / Q000378:metabolism* / Q000648:ultrastructure; D015221:Potassium Channels / Q000187:drug effects / Q000235:genetics*; D012996:Solutions; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D012996:Solutions; D013757:Tetraethylammonium Compounds; D014212:Tretinoin; D015761:4-Aminopyridine; D004121:Dimethyl Sulfoxide