Pharmacology of volume regulation following hypotonicity-induced cell swelling in clonal N1E115 neuroblastoma cells

When exposed to hypotonic solutions, clonal N1E115 neuroblastoma cells initially swell and later undergo a regulatory volume decreae (RVD). We studied the effects of a variety of transport inhibitors on the time course of cross-sectional area of N1E115 cells exposed to a solution of reduced osmolari...

Full description

Saved in:
Bibliographic Details
Published in:Brain research 1995-07, Vol.686 (1), p.29-36
Main Authors: Lippmann, Bruce J., Yang, Roger, Barnett, David W., Misler, Stanley
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Bumetanide
Cell physiology
Cell Size - drug effects
Chloride Channels - antagonists & inhibitors
Cl − channel blocker
Clone Cells - drug effects
Cytosolic Ca 2
Fundamental and applied biological sciences. Psychology
Hypotonic Solutions
Ion Transport - drug effects
K + channel blocker
Mice
Miscellaneous
Molecular and cellular biology
Neuroblastoma
Neurons - drug effects
Osmolar Concentration
Ouabain
Potassium Channel Blockers
Regulatory volume decrease
Stretch-activated channel blocker
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:When exposed to hypotonic solutions, clonal N1E115 neuroblastoma cells initially swell and later undergo a regulatory volume decreae (RVD). We studied the effects of a variety of transport inhibitors on the time course of cross-sectional area of N1E115 cells exposed to a solution of reduced osmolarity ( π = 186mosm). Application to the bath of either: (i) blockers of net K efflux through K channels (e.g. isotonic KCl or 20 mM TEA); or (ii) blockers of net efflux through anion channels (e.g. isotonic methanesulfonate, 10 μM DIDS or 100 μM IAA-94) all prevent RVD. In contrast, ouabain (a Na +/K + pump blocker), bumetanide (a Na +/K +Cl − cotransporter blocker) and SITS (a HCO 3 −/Cl − exchange blocker) do not. These data support the involvement of these channels over pumps or exchangers in solute exit during RVD. Only variable block of RVD was achieved using blockers of stretch activated non-selective cation C +(SA) channels (i.e., amiloride and gadolinium, Gd 3+) or a membrane permeant Ca chelator (BAPTA-AM) suggesting that neither the opening of C +(SA) channels nor a global rise in cytosolic Ca 2+ is critical for triggering RVD.
ISSN:0006-8993
1872-6240
DOI:10.1016/0006-8993(95)00447-X