[unreadable] Rats will suppress intake of a saccharin solution that predicts either passively administered or self-administered drugs of abuse. For many years it was believed that drugs of abuse were actually producing a conditioned taste aversion, similar to that induced by lithium chloride. However there is substantial evidence to suggest that the suppressive effects of drugs of abuse are actually caused by a devaluation of the natural reinforcer in anticipation of the more potent drug reward--a reward comparison (Grigson, 1997). Little is known about the neural substrates involved this phenomenon, however recent studies have shown that lesions of the gustatory thalamus disrupt the suppressive effects of passively administered cocaine or morphine. Additionally, the classical conditioning involved in reward comparison suggests the involvement of the amygdala, a region thought to be important for both appetitive and aversive associative learning. The involvement of this region is also supported by anatomical findings of a strong projection from the gustatory pathway to the central nucleus of the amygdala. Using lesion techniques, the proposed experiments will examine the contribution of the gustatory thalamus and central nucleus of the amygdala to the suppressive effects of drugs of abuse (Specific Aim 1). The neurochemical basis of these contributions will then be examined via microinfusion techniques (Specific Aim 2). [unreadable] [unreadable] [unreadable] [unreadable]