Role of the Gustatory Thalamus in Taste Learning

Lesions of the gustatory thalamus (GT) completely eliminate morphine-induced conditioned taste aversions (CTAs) but have no influence on illness-induced CTAs. This lesion-based dissociation has been used to support hypotheses characterizing drug-induced taste learning as taste avoidance rather than taste aversion. However, proper comparison of lesion effects across these studies is compromised by procedural differences. The illness-induced CTA literature tends to use longer taste access periods (e.g., 15-min) whereas all investigations of morphine-induced CTA in GT-lesioned (GTX) rats have used 5-min access periods. In order to compare lesion effects the present research used a standard 15-min taste access period and examined GTX rats in morphine-induced CTA (Experiment 1) and lithium chloride-induced CTA (Experiment 2). To examine the generality of drug effects a second set of GTX rats were tested in an amphetamine-induced CTA (Experiment 3). These rats were also tested for the occurrence and habituation of taste neophobia (Experiment 4). The results clearly demonstrated that GT lesions do not eliminate drug-induced CTA with either morphine or amphetamine. Rather, it appeared that GTX rats acquired drug-induced CTA normally but from an elevated Trial 1 starting point. GT lesions had no influence on the acquisition of an illness-induced CTA despite elevating Trial 1 intake. Lesion-induced overconsumption of a novel taste solution was consistently found across all four experiments, a deficit that has not previously been attributed to GT lesions. The present results show that the GT has little if any role in CTA acquisition and revealed an involvement in taste neophobia that has not previously been described.