Effect of a toxin isolated from the sponge Haliclona viridis on the release of gamma-aminobutyric acid from rat olfactory bulb.

A partially purified toxin from the marine sponge Haliclona viridis was studied for its effect on the presynaptic release mechanism of 3H-gamma-aminobutyric acid from nerve terminals of the external plexiform layer of rat olfactory bulb. Previously, the toxin of H. viridis was shown to block the resting potassium conductance in frog muscle. In the present study, the toxin induced a reversible release of 3H-gamma-aminobutyric acid in the external plexiform layer. This effect was similar to that induced by 25 mM K+. The toxin-induced outflow of 3H-gamma-aminobutyric acid was concentration dependent. The action of the toxin was specific for gamma-aminobutyric acid secretion from the external plexiform layer, and dopamine liberation from the frontal cortex; the toxin did not release 3H-valine, a non-neurotransmitter amino acid, from the external plexiform layer. Toxin- and high K(+)-induced neurotransmitter release were both drastically reduced when Ca2+ was removed from the saline. The addition of 0.3 microM tetrodotoxin or the removal of Na+ from the saline did not reduce the toxin's ability to release neurotransmitters. The effect of toxin was enhanced by the addition of valinomycin. Although Haliclona toxin and 4-aminopyridine induced the release of neurotransmitters, they antagonized each other's effect on gamma-aminobutyric acid secretion when added simultaneously.