Signalling and incentive processes in instrumental reinforcer devaluation.

We have previously reported that conditioning an aversion to the reinforcer using an isotonic lithium chloride (LiCl) solution following instrumental training reduces performance in a subsequent extinction test only if animals are re-exposed to the reinforcer prior to the test. Rescorla (1992), in contrast, reported an immediate devaluation effect using a hypertonic LiCl solution that did not depend upon re-exposure. In two experiments we examined the effect of using a hypertonic LiCl solution to condition the aversion to the reinforcer on subsequent instrumental performance in extinction, with and without re-exposure. In Experiment 1 thirsty rats were trained to press a lever for a sucrose solution before being injected with 0.6 M LiCl either immediately or after a delay. Half of the immediate and delay groups were then re-exposed to the sucrose in the absence of the lever, with the remainder being exposed to water. Contrary to the previously reported effects of isotonic LiCl, a hypertonic solution induced a reinforcer devaluation effect in all the immediately poisoned animals, which did not depend upon re-exposure to the reinforcer. In Experiment 2 the possibility that this devaluation effect was induced by the discomfort associated with the hypertonicity of the solution was assessed by replicating Experiment 1 but, in addition, using two immediately poisoned groups given the LiCl injection under anaesthesia. In the absence of anaesthesia, the devaluation effect observed without re-exposure to the reinforcer in Experiment 1 was replicated. When the injection was given under anaesthesia, however, a reinforcer devaluation effect was observed only in animals that were re-exposed to the reinforcer prior to the extinction test. These results were interpreted as evidence that a reinforcer devaluation effect induced by pairing the reinforcer with illness depends upon a process of incentive learning, whereas a devaluation effect mediated by learning a signalling relationship between the reinforcer and somatic discomfort does not.