The present study re-examined the involvement of the gustatory thalamus (GT) in the acquisition of drug- and toxin-induced conditioned taste aversions (CTAs) using a standardized procedure involving 15-min taste trials in rats injected with morphine (Experiment 1), lithium chloride (Experiment 2) or amphetamine (Experiment 3). Contrary to previous results, GT lesions did not eliminate drug-induced CTAs. Rather, GT-lesioned rats acquired aversions of comparable magnitude to non-lesioned subjects but from an elevated intake on the first conditioning trial. A similar pattern of lesion effects was found in the acquisition of an illness-induced CTA. Thus, we conclude that GT lesions do not differentially influence CTAs conditioned with drugs or toxins. The lesion-induced elevated intake of a novel tastant confirms an unappreciated role for the GT in taste neophobia.