The role of taurine in the regulation of brain cell volume in chronically hyponatraemic rats

Cells in slices prepared from the superficial cerebral cortex of normonatraemic rats underwent moderate swelling when exposed to low Na+ medium (122 mmol/l) accompanied by a large increase in the rate of efflux of preloaded taurine. In contrast, cells in slices from chronically (4 day) hyponatraemic rats did not increase in volume and the rate of taurine efflux was unchanged. The anion transport inhibitor 4,4'-diisothiocyanato-stilbene-2,2'-sulphonic acid (25 mu mol/l) caused marked (-44%) reduction in taurine efflux in cells from normonatraemic rats; this response was strongly attenuated (-16%) by hyponatraemia. When slices from hyponatraemic rats were acutely exposed to medium containing 142 mmol/Na+ cells exhibited marked and paradoxical swelling. This response was completely abolished by the NaCl co-transport inhibitor bumetanide (50 mu mol/l) and was not observed in slices that had not been pre-loaded with taurine. Forty eight hours after the start of the remission of hyponatraemia, cells from post-hyponatraemic rats displayed normal responses (i.e., moderate swelling and greatly accelerated taurine efflux) on exposure to 122 mmol/Na+. But at 24 h there was only partial restoration of the efflux response to 122 mmol/Na+, with an enhanced cell swelling response that was not significantly affected by bumetanide. II is concluded that (i) during chronic hyponatraemia, unlike acute hyposmotic stress, cortical cells preserve their volume and that this is not associated with any increase in the rate of taurine loss; there does however, appear to be a decrease in the anionic component of cellular taurine efflux; (ii) acute re-incubation of slices in medium containing 142 mmol/l Na+ is associated with cell swelling that may reflect up-regulation of Na/Cl/taurine co-transport; (iii) following restoration of normonatraemia the pattern of normal cellular response to acute hyposmotic stress is only gradually re-established. (C) 1998 Elsevier Science Ltd. All rights reserved.