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Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization

Collard, K.J., Wilkinson, Lawrence Stephen ORCID: and Lewis, D.J. 1988. Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization. British Journal of Pharmacology 93 (2) , pp. 341-348. 10.1111/j.1476-5381.1988.tb11440.x

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1 The efflux and influx of tryptophan across the synaptosomal plasma membrane has been studied under a variety of experimental conditions, in order to examine the mechanism by which depolarization enhances the efflux of tryptophan from superfused synaptosomes. 2 Efflux of [3H]-tryptophan from preloaded superfused synaptosomes was found to be enhanced by K+ depolarization in a Ca2+ and dose-dependent manner. In contrast, [3H]-phenylalanine efflux was only poorly stimulated by depolarization and only by very high concentrations of K+. 3 Tryptophan efflux was also enhanced by decreasing the extracellular Na+ concentration, but this effect was not dependent on extracellular Ca2+. 4 Influx of [3H]-tryptophan into synaptosomes was stimulated by extracellular Na+ removal, but the uptake of [3H]-phenylalanine was unaffected by this procedure. 5 Both the induced influx and efflux of tryptophan observed under these experimental conditions was inhibited by immobilizing the plasma membrane carrier with parachlorophenylalanine. This implied that both the enhanced influx and efflux arose as a consequence of the activation of the membrane tryptophan carrier, the direction of the observed effect being dependent upon the manner in which the experiments were conducted. 6 The relationship between depolarization, the activation of the membrane tryptophan carrier and the significance of this to the in vivo situation is discussed.

Item Type: Article
Date Type: Publication
Status: Published
Schools: MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > R Medicine (General)
Publisher: Nature Publishing Group
ISSN: 0007-1188
Last Modified: 31 Oct 2022 10:36

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