Effects of anion channel blockers on hyposmotically induced amino acid release from the in vivo rat cerebral cortex

A cortical cup model with continuous perfusion of artificial cerebrospinal fluid (containing 134 mM NaCl) was used to investigate the effects of anion channel blockers on the hyposmotically-induced release of amino acids from the in vivo rat cerebral cortex. The hyposmotic stimulus (25 mM NaCl) evok ed a release of taurine, glutamate, aspartate, glycine, phosphoethanolamine and GABA. Topically applied anion channel blockers 4,4'-diisothiocyanatost ilbene-2,2'-disulfonic acid (1 mM); 4-acetamido-4'-isothiocyanatostilbene-2 ,2-disolfonic acid (2 mM); 5-nitro-2-(3-phenylpropylamino) benzoic acid (35 0 mu M); niflumic acid (500 mu M); tamoxifen (20 mu M) and arachidonic acid (0.5 mu M) all significantly reduced the hyposmotically-induced release of taurine. The releases of glutamate, aspartate, glycine, phosphoethanolamin e and GABA were variably susceptible to inhibition by these compounds. Thes e results demonstrate that osmoregulatory processes in cortical cells, in v ivo, involve amino acids, with taurine playing a dominant role. The efflux of taurine and, to a lesser extent, the other amino acids may be mediated b y anion channels.