Asymmetric ibotenic acid lesions of the taste nuclei in the thalamus and cortex (THCx) selectively disrupt avoidance of a taste cue when paired with a rewarding sucrose solution or morphine, but not when paired with the aversive agent, LiCl (Geddes et al., submitted). The present study used similar THCx lesions to examine the role of this thalamocortical loop in drug-induced suppression of intake of the taste cue, drug-seeking (runway) and drug-taking (self-administration) behavior. Using predetermined coordinates (cortex) and electrophysiological guidance (thalamus), 22 rats received unilateral lesions of the VPMpc and contralateral lesions of the gustatory insular cortex (THCx). The remaining 22 control (Cntl) rats received ipsilateral lesions (different nuclei, same hemisphere). In Experiment 1, half of the Cntl and THCx rats were water-deprived and given 5 min access to saccharin in the start box followed by an ip injection of morphine (15 mg/kg) in the goal box for 6 trials in a runway. In Experiment 2, the remaining half of the rats were water-deprived and given 5 min access to the saccharin CS followed by 1.5 h to self-administer cocaine over 14 trials in an operant chamber. Collectively, the results showed that the THCx lesion blocked both morphine- and cocaine-induced suppression of intake of the saccharin CS, but had no effect on instrumental responding for the drug. Thus, while this thalamocortical loop is essential for drug-induced devaluation of CS intake, it is not involved in responding, instrumentally, to the reinforcing properties of the drugs. This research was supported by DA12473 and DA017416.