ABSTRACT
In the animal world certain species use specific biological weapons (e.g. neurotoxins) to paralyze the nervous system of their victim by blocking synaptic transmission. For understanding the molecular mechanism of the neurotransmitter release these toxins serve as useful pharmacological tools. Such a tool is for instance alpha latrotoxin (α-LTX), a 116-130 kDa protein component of the venom of black widow spiders. This toxin selectively toxic for vertebrate presynaptic secretary apparatus. α-LTX induces a massive release of several neurotransmitters (e.g. acetylcholine, γ-aminobutyric acid (GABA), noradrenaline, dopamine, glutamate) at both peripheral and central synapses, however, the precise molecular mechanism of this action has not been revealed yet. During the toxin action three phases can be identified. (1) The toxin binds to its presynaptic plasma membrane receptors, (2) forms a cation selective channel and (3) triggers the subsequent fusion of vesicles with the membrane. In this article we are focusing on the role of the external ions, especially the effect of divalent cations in each step of the action of α-LTX. Several other aspects of the α-LTX action has been extensively reviewed in the last 15 years (Hurlbut and Ceccarelli, 1979; Scheer et al., 1984; Grasso, 1988; Rosenthal and Meldolesi, 1989; Petrenko, 1993; Surkova, 1994).
