alpha-Latrotoxin-stimulated GABA release can occur in Ca(2+)-free, Na(+)-free medium.

We have studied [14C]GABA release from synaptosomes induced by native and monoclonal antibodies-modified alpha-latrotoxin (LTX). Modification of LTX eliminates the toxin's ability to increase [Ca2+]i influx into synaptosomes. It has been shown that native LTX does not change 22Na influx into rat brain synaptosomes. Both toxin forms studied, native and modified by monoclonal antibodies, stimulate [14C]GABA release from synaptosomes in divalent-free medium where sodium was substituted by equimolar concentrations of choline chloride. Native toxin induces a more rapid stimulation of [14C]GABA release than the modified one. It was suggested that the difference in the mediator release rates is not accounted for by the inability of modified toxin to form active ion channels in synaptosomal plasmalemma, but most probably by the state of toxin-receptor complexes.