Characterization of transmitter release as a response of vertebrate neural tissue to erythrosin B.

A rat cerebral cortical slice preparation was used to study the response of transmitter release to the application of the food dye, Erythrosin B, a tetraiodinated derivative of fluorescein. Erythrosin B (100 microM) stimulated net release of previously taken up [3H]norepinephrine and [3H]gamma-aminobutyric acid (GABA). The Erythrosin-induced release of GABA (the only transmitter studied) occurred in the absence of added Ca2+, and in the presence of tetrodotoxin (TTX). Ultrastructural analysis of the vesicle content of frog neuromuscular junctions treated with Erythrosin B revealed a diminution in the number of synaptic vesicles present in the nerve terminal. By using fluorescein and some halogen-substituted derivatives including Erythrosin B, it was found that incubation with the unhalogenated compound caused no net release, whereas incubation with the iodine-, chlorine- or bromine-substituted compound did cause release. It was also found that somewhat greater release induced by Erythrosin B (at 100 microM) occurred in the light than in the dark. That Erythrosin B inhibits the Na+,K+,Mg2+-ATPase was confirmed in this preparation; it did so in both light and dark. The discrepancy between release and Na+,K+,Mg2+-ATPase blockade in the dark suggests that release either occurs by some other mechanism than by Na+,K+,Mg2+-ATPase blockade, or that an additional light-dependent process contributes to the release. We conclude that Erythrosin B can presumably induce net release of transmitters generally, that release does not occur via the TTX-sensitive Na+ channel, that release via vesicles does occur, and that light somewhat enhances the release.