Dr. J. A. Hardy is Department of Biochemistry, St. Mary's Hospital Medical School, Paddington, London W2 1PG, U.K.
Efflux of Putative Transmitters from Superfused Rat Brain Slices Induced by Low Chloride Ion Concentrations
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 48, Issue 4, pages 1060–1068, April 1987
How to Cite
Turner, J. D., Boakes, R. J., Hardy, J. A. and Virmani, M. A. (1987), Efflux of Putative Transmitters from Superfused Rat Brain Slices Induced by Low Chloride Ion Concentrations. Journal of Neurochemistry, 48: 1060–1068. doi: 10.1111/j.1471-4159.1987.tb05627.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received September 12, 1985; revised September 13, 1986; accepted September 26, 1986
- Neurotransmitter efflux;
- Superfused brain slices;
- Low chloride-containing media)
Abstract: Slices of rat cerebral cortex, preloaded with [14C]γ-aminobutyric acid (GABA) and either [3H]5-hy-droxytryptamine (5-HT) or [3H]noradrenaline, were super-fused with media in which varying concentrations of Cl−had been replaced with other monovalent anions. Rapid reduction of [Cl″], by superfusion with media containing instead the impermeant anions propionate, isethionate, glu-conate, or methyl sulphate, caused increases in the efflux of tritiated biogenic amines, but the increase in that of [14C]-GABA was not significant. The increased efflux of [3H]5-HT evoked by superfusion with low Cl− levels when propionate was the replacement anion, was transient and was linearly related to the log[Cl−]−1. It was not affected by removal of Ca2+ or by addition of 10 mM Mg2+ and was delayed but not abolished by tetrodotoxin. The low C1–-evoked efflux of [3H]5-HT was not affected by pretreatment with neuronal reuptake blockers but was inhibited by picrotoxin, strychnine, and 4-acetamido-4-isothiocyanostilbene-2,2-disul-phonic acid and was enhanced by glycine. Muscimol and GABA were without effect. These observations are taken to indicate that the efflux of biogenic amines is brought about by terminal depolarisation due to outward movement of Cl−in low chloride-containing media. They are of relevance to other physiological and pharmacological studies in which anion concentrations are manipulated and suggest that the anion-evoked release phenomenon may provide a model for the analysis of Cl−-dependent mechanisms in nerve terminals.