Abstract
Abstract
Scorpion toxin, a substance that induces neurotransmitter release by depolarizing neurons, was used to stimulate amylase release from guinea pig pancreatic lobules. Scorpion toxin was found to act selectively on acinar cell neurons but not directly on acinar cells. The toxin's action on lobules was blocked by tetrodotoxin, whereas scorpion toxin itself had no effect on isolated pancreatic acini. Toxin-induced amylase secretion from pancreatic lobules included two components, one that was atropine sensitive and one that was atropine resistant. This finding is consistent with the notion that scorpion toxin releases cholinergic and noncholinergic transmitters. Both cholinergic and noncholinergic effects showed a similar dose dependence, being maximal at a toxin concentration of 3 μg/ml. The noncholinergic pathway was not mediated through the CCK receptor since it was not blocked by dibutyryl cyclic GMP, a CCK antagonist. Moreover, the noncholinergic mechanism appeared to have a different biochemical mechanism of action than CCK in that scorpion toxin in the presence of atropine did not release rapidly intracellular Ca2+ prelabeled with 45Ca2+. The results suggest, therefore, the existence of a second neurotransmitter present in pancreatic nerve endings capable of stimulating amylase release in the guinea pig.
Get full access to this article
View all access options for this article.