Abstract
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 μM) stimulated net release of previously taken up [
3H]norepinephrine and [
3H]γ-aminobutyric acid (GABA). The Erythrosin-induced release of GABA (the only transmitter studied) occured in the absence of added Ca
2+, 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 found that somewhat greater release induced by Erythrosin B (at 100 μM) occurred in the light than in the dark. That Erythrosin B inhibits the Na
+, K
+, Mg
2+-ATPase was confirmed in this preparation; it did so in both light and dark. The discrepancy between release and Na
+, K
+, Mg
2+-ATPase blockade in the dark suggests that release either occurs by some other mechanism than by Na
+, K
+, Mg
2+-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.