In situ localization and osmotic regulation of the sodium/ myo
-inositol cotransporter in rat brain.
Ibsen, Laura, and Kevin Strange.
Critical Care Research Laboratories, Departments of Medicine
(Nephrology) and Anesthesia, Children's Hospital, Harvard Medical
School, Boston, MA 02115
APStracts 3:0127F, 1996.
Organic osmolytes accumulate in the mammalian brain when plasma
osmolality is elevated chronically. An understanding of organic
osmolyte regulation is important for elucidating the pathophysiology
of numerous disease states, particularly those in which plasma
osmolality is altered or manipulated. To this end, we have previously
characterized the mechanisms of osmoregulatory myo-inositol
accumulation and loss in rat brain glial cells. The validity of cell
culture models of physiological functions, however, requires
demonstration of similar behavior in vivo. We therefore examined the
effect of serum hypertonicity and its correction on expression of the
Na+/myo-inositol cotransporter (SMIT) in rat brain. Northern analysis
revealed that chronic serum hypertonicity increased brain SMIT mRNA
levels 4-7 fold. Rapid reduction of serum osmolality caused a rapid
fall in SMIT mRNA levels. In situ hybridization revealed a widespread
distribution of cells expressing SMIT with striking regional
variability in the number of and intensity of cells labeled. These
results confirm and extend our studies of cultured glial cells and
indicate that myo-inositol accumulation in vivo is due to increased
expression of SMIT. Regional variability in the distribution of SMIT
may be a factor in the differential vulnerability of certain brain
regions to shifts in plasma osmolality.
Received 15 May 1996; accepted in final form 11 July 1996.
APS Manuscript Number F150-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996