Veterinary and Biomedical Sciences, Department of
Document Type
Article
Date of this Version
5-23-2000
Citation
Published in Journal of Neuroscience Research 61:6 (September 2000), pp. 701–711; doi: 10.1002/1097-4547(20000915)61:63.0.CO;2-T.
Abstract
The efflux of potassium (K+) and amino acids from hippocampal slices was measured after sudden exposure to 10% (270 mOsm), 25% (225 mOsm) or 50% (150 mOsm) hyposmotic solutions or after gradual decrease (22.5 mOsm/min) in external osmolarity. In slices suddenly exposed to 50% hyposmotic solutions, swelling was followed by partial (74%) cell volume recovery, suggesting regulatory volume decrease (RVD). With gradual hyposmotic changes, no increase in cell water content was observed even when the solution at the end of the experiment was 50% hyposmotic, showing the occurrence of isovolumic regulation (IVR). The gradual decrease in osmolarity elicited the efflux of 3H-taurine with a threshold at –5 mOsm and D-[3H]aspartate (as marker for glutamate) and at –20 mOsm for [3H]GABA. The efflux rate of [3H]taurine was always notably higher than those of [3H]GABA and D-[3H]aspartate, with a maximal increase over the isosmotic efflux of about 7-fold for [3H]taurine and 3- and 2-fold for [3H]GABA and D-[3H]aspartate, respectively. The amino acid content in slices exposed to 50% hyposmotic solutions (abrupt change) during 20 min decreased by 50.6% and 62.6% (gradual change). Taurine and glutamate showed the largest decrease. An enhancement in 86Rb efflux and a corresponding decrease in K+ tissue content was seen in association with RVD but not with IVR. These results demonstrate the contribution of amino acids to IVR and indicate their involvement in this mechanism of cell volume control.
Included in
Biochemistry, Biophysics, and Structural Biology Commons, Cell and Developmental Biology Commons, Immunology and Infectious Disease Commons, Medical Sciences Commons, Veterinary Microbiology and Immunobiology Commons, Veterinary Pathology and Pathobiology Commons
Comments
Copyright © 2000 Wiley-Liss, Inc. Used by permission.