Osmoregulatory changes in Myo-inositol content and Na+/Myo-inositol contransport in rat cortical astrocytes
Article first published online: 12 OCT 2004
Copyright © 1994 Wiley-Liss, Inc.
Volume 12, Issue 1, pages 35–43, September 1994
How to Cite
Strange, K., Emma, F., Paredes, A. and Morrison, R. (1994), Osmoregulatory changes in Myo-inositol content and Na+/Myo-inositol contransport in rat cortical astrocytes. Glia, 12: 35–43. doi: 10.1002/glia.440120105
- Issue published online: 12 OCT 2004
- Article first published online: 12 OCT 2004
- Manuscript Accepted: 31 MAR 1994
- Manuscript Received: 25 JAN 1994
- Volume regulation;
- Organic osmolytes;
- Brain volume;
Exposure of cortical astrocytes to 325, 350, or 390 mosM culture media for 48 h caused a 1.4-, 2.1-, and 3.5-fold increase, respectively, in cellular content of the compatible osmolyte myo-inositol. Elevated myo-inositol levels accounted for ∼56-100% of the solute needed by the cells for complete volume regulation under hypertonic conditions. Myo-inositol accumulation was associated with 4-5-fold (peak rate) and 1.8-2-fold (steady-state rate) increases in the rate of Na+ -dependent myo-inositol uptake when cells were acclimated to 390 mosM culture medium for 12 h or 24-96 h, respectively. When medium osmolality was elevated by 25 mosM, peak and steady-state increases in myo-inositol uptake of 1.7-fold and 1.3-fold, respectively, were observed. Exposure to 390 mosM medium for 12-48 h induced a 3-8-fold increase in cotransporter mRNA levels suggesting that the increase in myo-inositol uptake is brought about by increased cotransporter gene expression. Abrupt return of hypertonic cells to an isotonic medium induced a rapid increase in myo-inositol efflux and a return of cotransporter mRNA to control values in <2 h. In contrast, the cotransporter remained fully activated at hypertonic levels for 16 h. Between 16-24 h after the transfer, the rate of myo-inositol uptake returned to control values. The remarkable sensitivity of the cotransporter to hypertonic stress indicates that upregulation of myo-inositol transport in glial cells is likely to occur in a variety of disease states that cause an elevation of plasma osmolality. Slow downregulation of the cotransporter may be responsible in part for the slow loss of myo-inositol and cerebral edema that occurs with too rapid correction of chronic plasma hypertonicity.