Hypothetical explanation of the experimental data showing differences in taurine and glutamate release <i>in vivo</i>.

Abstract

<p>A reduction in medium osmolarity (↓[osm]_e) in the rat cortex causes an increase in the extracellular levels of the excitatory amino acids glutamate and aspartate and the sulfonic acid taurine via a mechanism sensitive to the anion channel blocker DNDS. Despite these similarities, the excitatory amino acid and taurine release demonstrate different kinetics and are likely mediated by different transport pathways (1 and 2) and/or originate from different cellular sources. The taurine pathway (1) but not the excitatory amino acid pathway (2) is activated by isoosmotic lowering of [NaCl]_e. Conversely, the swelling-activated excitatory amino acid release pathway (2) but not the taurine pathway (1) is potentiated by H₂O₂. Alternative transport pathways that were considered in this study include: [Na⁺]_e-dependent taurine transporters (3), [Na⁺]_e/[K⁺]_i-dependent glutamate transporters in neurons (4), and in astrocytes (5), which are sensitive to TBOA; and vesicular glutamate release (6), which is sensitive to the voltage-gated Ca²⁺ channel blocker Cd²⁺. Based on the similarities of excitatory amino acid release <i>in vivo</i> and in cultured astrocytes, we speculate that glutamate release <i>in vivo</i> largely originates from glial cells. Similarities between taurine release <i>in vivo</i> and in synaptosomes suggest that taurine release may be of a neuronal origin.</p