We have studied [C-14]GABA release from synaptosomes induced by native
and monoclonal antibodies-modified alpha-latrotoxin (LTX). Modificati
on of LTX eliminates the toxin's ability to increase [Ca2+](i) influx
into synaptosomes. It has been shown that native LTX does not change N
a-22 influx into rat brain synaptosomes. Both toxin forms studied, nat
ive and modified by monoclonal antibodies, stimulate [C-14]GABA releas
e from synaptosomes in divalent-free medium where sodium was substitut
ed by equimolar concentrations of choline chloride. Native toxin induc
es a more rapid stimulation of [C-14]GABA release than the modified on
e. 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 st
ate of toxin-receptor complexes.