Conditioned taste aversions: Vagal and circulatory mediation of the toxic unconditioned stimulus

Abstract

In these experiments we tested the hypothesis that the same afferent systems which mediate vomiting reflexes also participate in conditioned taste aversions which are formed when ingestion of a taste cue is paired with subsequent internal malaise. Borison and Wang have shown that emetic reflexes in dogs and cats are integrated in a brainstem center which responds to local gastric irritation mediated by the vagus or to bloodborne toxins monitored by brain stem chemoreceptors. This same afferent system may mediate taste-illness conditioning since the emetic center is anatomically associated with the relay nucleus for primary taste afferents. We have shown that subdiaphragmatic vagotomy in rats disrupts the acquisition of a saccharin aversion induced by repeated conditioning trials with low doses of intragastric or intraperitoneal copper sulfate. In contrast, there is little effect on the aversion produced by a single, larger dose of copper sulfate injected directly into the blood via the tail vein, although vagotomized rats displayed an accelerated extinction pattern. These results parallel reports on the effect of vagotomy on vomiting reflexes in dogs and suggest a functional relationship between acute vomiting reflexes in dogs and suggest a functional relationship between acute vomiting reflexes which eject poison and chronic conditioned taste aversions which inhibit subsequent ingestion of poison; further, they provide evidence that these responses are subserved, at least in part, by similar neural mechanisms.