Abstract

The kinetics of efflux [ 3H]taurine have been examined in pre-loaded slices of rat cerebral cortex incubated in media of variable osmolality. Alterations in the rate of the slowest phase of efflux, considered to represent cellular loss, have been correlated with cell volumes, provisionally identified as the slice non-inulin space. Efflux was stimulated by reduction in medium osmolality, and impaired in hyperosmotic media; these variations were accompanied by moderate (non-osmometric) cell swelling and shrinkage, respectively. The rates of taurine efflux into media in which NaCl was partly replaced by sucrose, and measurement of the corresponding cell volumes, suggest that ionic strength, rather than osmolality or cell volume per se, may be a significant controlling factor. In both isosmolal and hyposmolal media efflux was significantly impaired by the anion transport inhibitor niflumic acid, with accompanying cell swelling, or by replacement of chloride by gluconate. In hyposmotic, but not isosmotic, media efflux was impaired, and cell volumes increased, in the presence of trifluoperazine or TMB-8, a reported blocker of intracellular calcium release, and the effects of niflumic acid and trifluoperazine on both variables were strongly additive. It is suggested that in both isosmotic and hyposmotic media taurine, efflux occurs by anionic transport, mainly through exchange with external chloride, whereas in hyposmotic media a second pathway is present, probably a volume-activated calmodulin-dependent channel.

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