Heroin addiction is a chronic relapsing disease of the brain caused by drug-induced neuroadaptations at the molecular and cellular levels [7, 8]. It is well known that many stress responsive systems in the CNS, including the peptides, their receptors, and stress-related hormones, are involved in drug cravings in humans [9, 10, 11], and drug-seeking behavior triggered by exposure to various stressors in animals [4]. More specifically, in response to stress, hypothalamic arginine vasopressin (AVP) which activates V1b receptors stimulates ACTH secretion from the corticotropes in the anterior pituitary [e.g., 12, 13, 14]. The AVP/V1b receptor system is widely distributed in the CNS, suggesting that it may be mediators of the actions of central stress responsive systems [15]. Indeed, there is a growing body of evidence suggesting that AVP activity in the amygdala is an important element in the neurobiology of stress-related behaviors in rodents [15]. Increased AVP gene expression in the amygdala is associated with early withdrawal from chronic exposure to opiates, and the selective AVP V1b (but not V1a) receptor antagonist attenuates heroin-seeking behavior induced by foot shock stress
