The broadly defined extended amygdala, which includes the bed nucleus of the stria terminalis and the central medial amygdala have been implicated in behavioral motivation and reward (Alheid and Heimer 1988). These nuclei are fundamental in avoidance learning, and projections from the extended amygdala to the lateral and medial divisions of the hypothalamus also support their role in the regulation of autonomic and somatosensory activities. These functions have been studied extensively with regard to their role in appetitive mechanisms and addiction. Thus, the extended amygdala is in a unique position to coordinate inputs from multiple limbic lobe regions in order to provide behavioral responses though its output channels (Heimer 2003). Dysfunction of the extended amygdala has been proposed to underlie changes in behavioral motivation for rewarding objects that manifest as (a) impulsive acts driven by pleasure and gratification and the positive reinforcing effects of drugs of abuse and (b) compulsive behavior that is produced through negative reinforcement to reduce the negative emotional state arising from substance dependence (Koob 2003).
