TOXIN PURIFIED FROM THE VENOM OF BLACK-WIDOW SPIDER AFFECTS THE UPTAKE AND RELEASE OF RADIOACTIVE GAMMA-AMINO BUTYRATE AND N-EPINEPHRINE FROM RAT-BRAIN SYNAPTOSOMES

A purified neurotoxin from the venom of black widow spider Latrodectus mactans tredecimguttatus, when tested on synaptosomes by means of a perfusion technique, stimulates the release of previously accumulated radioactive transmitters. Black widow spider toxin has also been shown to be a potent inhibitor of the uptake systems for γ‐aminobutyrate and N‐epinephrine. The release from synaptosomes of radioactive N‐epinephrine and γ‐aminobutyrate was rapidly increased by the presence of a low concentration of toxin (∼ 1 nM). The toxin does not appear to cause either non‐specific membrane damage or the release of a non‐transmitter substance like γ‐amino[14C]isobutyric acid. The venom‐induced release of γ‐aminobutyrate was shown not to be dependent on extracellular calcium concentration provided that sodium ions are present. By contrast, that of N‐epinephrine appeared to be Ca‐dependent. The release of γ‐aminobutyrate induced by the toxin is not modified by the presence in the perfusing fluid of tetrodotoxin, dithioerythritol and strontium ions, or by pretreatment of synaptosomes with diaminobutyrate. The mechanism of toxin‐induced release is different from that of a depolarization‐induced release. By correlating previous electrophysiological observations with the results obtained in this biochemical study it may be suggested that the toxin can be used in studies aimed at the identification of components specific to the presynaptic terminal membrane involved in neurotransmitter release. Copyright © 1979, Wiley Blackwell. All rights reserved